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1
Stanisic, Marijana, Rajko Hrvacevic, Zoran Paunic, and Stanko Petrovic. "Nephronophthisis and medullary cystic kidney disease complex." Vojnosanitetski pregled 62, no. 9 (2005): 683–88. http://dx.doi.org/10.2298/vsp0509683s.
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Background. Nephronophthisis and medullary cystic kidney disease complex refers to the genetic heterogeneous group of inherited tubulointerstital nephritis. Nephronophthisis comprises at last 3 clinical manifestations, has the autosomal recessive pattern of inheritance, appears early in life and is the most frequent inherited kidney disease that causes terminal renal failure in childhood, while medullary cystic kidney disease has the autosomal dominant pattern of inheritance, is less frequent, and terminal renal failure appears later in life. These two forms have similar clinical and morphological findings but extrarenal manifestations, the median ages of occurrence of terminal renal failure, and siblings presence help us distinguish these diseases. Case report. In this article we illustrated the case of a 20- years old patient with the suspicion of having complex nephornophthisis and medullary cystic kidney disease based upon mild renal failure, seen in routinely taken laboratory findings and bilateral cysts in corticomedullary region of the kidneys verified on abdominal ultrasound examination. Conclusion. This disease should rise suspicion in children or adolescents with progressive renal failure, a typical clinical manifestation, blood and urine samples results, bilateral cysts in the corticomedullary region of the kidneys seen during ultrasound examination of the kidneys and family inheritance.
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Bereczki, Dániel. "Stroke in chronic renal failure." Orvosi Hetilap 149, no. 15 (April 2008): 691–96. http://dx.doi.org/10.1556/oh.2008.28292.
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Chronic kidney diseases and cardiovascular diseases have several common risk factors like hypertension and diabetes. In chronic renal disease stroke risk is several times higher than in the average population. The combination of classical risk factors and those characteristic of chronic kidney disease might explain this increased risk. Among acute cerebrovascular diseases intracerebral hemorrhages are more frequent than in those with normal kidney function. The outcome of stroke is worse in chronic kidney disease. The treatment of stroke (thrombolysis, antiplatelet and anticoagulant treatment, statins, etc.) is an area of clinical research in this patient group. There are no reliable data on the application of thrombolysis in acute stroke in patients with chronic renal disease. Aspirin might be administered. Carefulness, individual considerations and lower doses might be appropriate when using other treatments. The condition of the kidney as well as other associated diseases should be considered during administration of antihypertensive and lipid lowering medications.
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Leroy, Xavier, Laurent Lemaitre, Alexandre De La Taille, Marc Hazzan, Bruno Delepaul, Jerome Couturier, and Bernard Gosselin. "Bilateral Renal Oncocytosis With Renal Failure." Archives of Pathology & Laboratory Medicine 125, no. 5 (May 1, 2001): 683–85. http://dx.doi.org/10.5858/2001-125-0683-browrf.
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Abstract Oncocytosis is a term recently used to describe diffuse renal involvement by numerous oncocytic nodules. We report herein a case of a 53-year-old man with end-stage renal disease requiring hemodialysis. His kidneys were involved by numerous tumors. Histologic examination revealed more than 100 oncocytomas and an associated papillary renal cell carcinoma in the right kidney.
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Oh, Soo, Rabeet Khan, and Ahmed Ziada. "Polycystic kidney disease." InnovAiT: Education and inspiration for general practice 13, no. 6 (April 1, 2020): 326–35. http://dx.doi.org/10.1177/1755738020910762.
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Polycystic kidney disease (PKD) is a monogenic, hereditary disorder of the kidneys that leads to fluid-filled cysts within the renal tubes. It is one of the most common causes of end-stage renal failure. There are two types, the more common autosomal dominant (ADPKD) and the rarer autosomal recessive (ARPKD). ADPKD mostly presents in adulthood, whereas ARPKD is usually detected during antenatal screening or as a neonate. This article will focus on key points to understand and consider for the holistic management of PKD.
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Rahmawati, Wiwit, Heru Muryawan, and Farah Prabowo. "Renal imaging in children with chronic kidney disease." Paediatrica Indonesiana 53, no. 4 (August 31, 2013): 193. http://dx.doi.org/10.14238/pi53.4.2013.193-9.
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Background Chronic kidney failure is a cause of death inchildren. Diagnosing chronic kidney disease is often made byclinical manifestations, laboratory findings and ultrasonographyor other imaging tests. Early detection of chronic kidney diseaseis needed for education and management of the disease.Objective To describe renal imaging findings and mortality inchildren with chronic kidney disease .Methods This was a cross-sectional study on children with kidneydiseases who were inpatients at Dr. Kariadi Hospital from January2008 to June 2011. Data were taken from medical records. Chronickidney disease was confirmed by clinical manifestations, laboratoryfindings, and radiologic imaging. Renal ultrasound findings weredetermined by the radiologist responsible at that time. Resultswere presented as ft:equency distributions.Results Of 37 chronic kidney disease cases, 27 were males and 10were females. Subjects' most common complaints were dyspnea (7out of 3 7) and edema (30 out of 3 7) . Renal ultrasound imaging ofsubjects with chronic kidney disease yielded the following findings:reduced cortico-medullary differentiation (30 out of 3 7), bilateralechogenic kidneys (21 out of 3 7), reduced renal cortex thickness(4 out of 37) and small-sized kidneys (4 out of 37) . Eight of the37 children died. These 8 subjects had the following radiologicimaging findin gs: both kidneys appeared small in size (4 out ofS),reduced 'renal cortex' thickness (4 out of 8), echogenic kidneys(6 out of 8), and reduced cortico-medullary differentiation (8out of8).Conclusion Renal ultrasound imaging of pediatric subjects withchronic kidney disease revealed findings of reduced corticomedullarydifferentiation, bilateral echogenic kidneys, reducedrenal cortex thickness, and small kidneys bilaterally.
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Fatima, Tanveer, Aurangzeb Afzal, and Sania Ashraf. "CHRONIC KIDNEY DISEASE." Professional Medical Journal 25, no. 06 (June 10, 2018): 887–91. http://dx.doi.org/10.29309/tpmj/2018.25.06.276.
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Introduction: Hemodialysis is a process of removal of waste products andtoxic substances from the body using an extracorporeal system. During the procedure, lotsof hemodynamic and metabolic changes occur in the body as a result of which patientsundergoing hemodialysis may suffer from complications both acutely during or just after dialysisas well as in long term. Objective: To determine the frequencies of various acute intradialyticcomplications in our hemodialysis patients. Study Design: Cross sectional survey. Setting:Lahore General Hospital, Lahore. Period: 3 months from May 2017 to July 2017. Method:End stage renal disease patients on regular hemodialysis in the dialysis unit of a tertiary carehospital. A total of 81 patients were included in the study. Patients with acute renal failure andacute on chronic renal failure were excluded from the survey. Results: Common complicationsobserved in our studied population included muscle cramps (70.7%), post dialysis fatigue(57.3%), back ache (56.1%), intradialytic shivering (57.3%), hypoglycemia (21.4%), hypotension(37.8%), hypertension (8.5%), headache (13.4%), vomiting (13.4%) and anaphylaxis in 2.4%.Conclusion: Hemodialysis is a complex procedure and can cause many complications mostof which are not life threatening. With proper monitoring and immediate treatment thesecomplications can be overcome without causing interruption in hemodialysis.
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Den Hartogh, Danja J., and Evangelia Tsiani. "Health Benefits of Resveratrol in Kidney Disease: Evidence from In Vitro and In Vivo Studies." Nutrients 11, no. 7 (July 17, 2019): 1624. http://dx.doi.org/10.3390/nu11071624.
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Different diseases and disorders that affect the kidneys include, but are not limited to, glomerulonephritis, diabetic nephropathy, polycystic kidney disease, kidney stones, renal fibrosis, sepsis, and renal cell carcinoma. Kidney disease tends to develop over many years, making it difficult to identify until much later when kidney function is severely impaired and undergoing kidney failure. Although conservative care, symptom management, medication, dialysis, transplantation, and aggressive renal cancer therapy are some of the current strategies/approaches to kidney disease treatment, new preventative targeted therapies are needed. Epidemiological studies have suggested that a diet rich in fruits and vegetables is associated with health benefits including protection against kidney disease and renal cancer. Resveratrol, a polyphenol found in grapes and berries, has been reported to have antioxidant, anti-inflammatory, antidiabetic, hepatoprotective, neuroprotective, and anti-cancer properties. The current review summarizes the existing in vitro and in vivo animal and human studies examining the nephroprotective effects of resveratrol.
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Cojocaru, Manole, Inimioara Cojocaru, Isabela Silosi, and Camelia Vrabie. "Kidney Damage in Autoimmune Diseases." Journal of Medical Biochemistry 29, no. 2 (April 1, 2010): 61–65. http://dx.doi.org/10.2478/v10011-010-0007-x.
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Kidney Damage in Autoimmune DiseasesRenal involvement in autoimmunity has many facets. Glomerular, tubular and vascular structures are targeted and damaged as a consequence of autoimmune processes. Immunologically mediated kidney diseases represent the third most common cause of end-stage renal failure (after diabetic and hypertensive nephropathies). Appropriate evalution of patients with immune-mediated kidney diseases requires a meticulous history and physical examination, with particular attention to the urinalysis, tests of renal function and often renal biopsy. The thorough clinician should personally review microscopic urinalysis in any case in which there is a reasonable index of suspicion of immune-mediated renal disease. In this article we propose to highlight recent developments, with particular reference to renal autoimmunity. Systemic lupus erythe-matosus affects many parts of the body: primarily the skin and joints, but also the kidneys. Goodpasture's syndrome involves an autoantibody that specifically targets the kidneys and the lungs. IgA nephropathy is a form of glomerular disease that results when immunoglobulin A (IgA) forms deposits in the glomeruli, where it creates inflammation. Future research could look for how the disease occurs, and how to easily test for its presence so that early treatment could be started.
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Bonavia, Anthony, and Kai Singbartl. "Kidney Injury and Electrolyte Abnormalities in Liver Failure." Seminars in Respiratory and Critical Care Medicine 39, no. 05 (October 2018): 556–65. http://dx.doi.org/10.1055/s-0038-1673616.
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AbstractThe liver and kidney are key organs of metabolic homeostasis in the body and display complex interactions. Liver diseases often have direct and immediate effects on renal physiology and function. Conversely, acute kidney injury (AKI) is a common problem in patients with both acute and chronic liver diseases. AKI in patients with acute liver failure is usually multifactorial and involves insults similar to those seen in the general AKI population. Liver cirrhosis affects and is directly affected by aberrations in systemic and renal hemodynamics, inflammatory response, renal handling of sodium and free water excretion, and additional nonvasomotor mechanisms. Subsequent problems, for example, worsening ascites, hyponatremia, and AKI, often complicate management of patients with chronic progressive liver disease and add to their morbidity and mortality. Thus, AKI must be carefully defined and diagnosed in patients with liver disease. The kidney also plays a pivotal role in balancing acid–base disturbances resulting from advanced liver disease, making AKI in the setting of end-stage liver disease very difficult to manage clinically. While renal dysfunction in these patients often resolves following orthotopic liver transplant, dialysis may be required as a bridge to transplantation to mitigate the metabolic disarray found in these critically ill patients.
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Kelly, Katherine J., Jizhong Zhang, Mingsheng Wang, Shaobo Zhang, and Jesus H. Dominguez. "Intravenous renal cell transplantation for rats with acute and chronic renal failure." American Journal of Physiology-Renal Physiology 303, no. 3 (August 1, 2012): F357—F365. http://dx.doi.org/10.1152/ajprenal.00680.2011.
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Acute kidney injury (AKI) and chronic renal failure (CKD) are the most challenging problems in nephrology. Multiple therapies have been attempted but these interventions have minimal effects on the eventual outcomes, and all too often the result is end-stage renal disease (ESRD). The only effective therapy for ESRD is renal transplantation but only a small fraction of patients receive transplants. In this work we introduce a novel approach to transplantation designed to regenerate kidneys afflicted by severe AKI or CKD: intravenous renal cell transplantation (IRCT) with adult rat primary renal cells reprogrammed to express the SAA gene localized and engrafted in kidneys of rat recipients that had severe AKI or CKD. IRCT significantly resolved renal dysfunction and limited kidney damage, inflammation, and fibrosis. Severe CKD was successfully improved by IRCT using kidney cells from donor rats or by renal cell self-donation in a form of autotransplantation. We propose that IRCT with adult primary renal cells reprogrammed to express the SAA gene can be used to effectively treat AKI and CKD.
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Nunes, Camilla Magnoni Moretto, Camila Lopes Ferreira, Daniella Vicensotto Bernardo, Andréa Carvalho De Marco, Mauro Pedrine Santamaria, and Maria Aparecida Neves Jardini. "Chronic kidney disease and periodontal disease. Case report." Brazilian Dental Science 21, no. 1 (March 28, 2018): 133. http://dx.doi.org/10.14295/bds.2018.v21i1.1498.
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<p>Chronic renal disease promotes a decrease on kidneys filterability and nitrogen products accumulation on blood, electrolyte and system endocrine functions imbalance. Among the many clinical manifestations of chronic renal failure (CRF) in the oral cavity, there are: dry mouth, uremic stomatitis, radiographic changes in maxillary and jaw bones and accumulation of calculus on the teeth that increases levels of periodonto pathogenic microorganisms able to lead a periodontal tissue destruction and also have the potential to act from a distance on other organs, e.g. the kidneys. Thus, it becomes evident that a periodontal treatment of patients suffering from chronic renal failure is crucial for maintaining their general health conditions and a subsequent successful organ transplant.Thus, the objectives of this case report were to highlight how important the periodontal treatment is for chronic renal failure patients and to demonstrate improvements in their clinical condition through the treatment plan proposed herein. A patient with 43 years old carrier generalized moderate chronic periodontitis and CRF was submitted to scaling and root planning sessions, and later surgical access for scaling where the basic treatment not resulted in a resolution of the inflammatory periodontal process. The results obtained from a well-developed periodontal treatment and an effective cooperation of patient showed satisfactory results with periodontal disease process resolution or stabilization.Thus, periodontal treatment and patient compliance were crucial for the improvement of periodontal clinical conditions enabling a future successful renal transplantation.</p><p><strong>Keywords</strong></p><p>Dental care; Periodontal diseases; Renal insufficiency.</p>
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Harris, D. C., L. Chan, and R. W. Schrier. "Remnant kidney hypermetabolism and progression of chronic renal failure." American Journal of Physiology-Renal Physiology 254, no. 2 (February 1, 1988): F267—F276. http://dx.doi.org/10.1152/ajprenal.1988.254.2.f267.
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To investigate the mechanisms whereby verapamil and dietary phosphate restriction slow progression of nephron loss after renal ablation, the effects of these maneuvers on inulin clearance (CIn), net sodium reabsorption (TNa+), oxygen consumption (QO2), and net glucose production (GP) were examined in isolated perfused normal and remnant kidneys. Preliminary studies characterized the isolated perfused remnant kidney perfusion. Adaptation to renal ablation was greater for QO2 (102% of normal), GP (138%), and kidney weight (79%) than CIn (51%) or TNa+ (40%). Verapamil (50 microM) lowered QO2 in remnant kidneys (1.64 +/- 0.24 vs. control 2.86 +/- 0.16 mumol.min-1.g-1, P less than 0.005), as did phosphate restriction (1.81 +/- 0.22 vs. control 3.05 +/- 0.40 mumol.min-1.g-1, P less than 0.05). These effects could not be accounted for by changes in CIn, TNa+, or GP and were not observed in normal kidneys. In summary 1) remnant kidneys are hypermetabolic compared with normal kidneys when assessed by QO2 and GP; 2) verapamil and phosphate restriction diminish the enhanced metabolic activity of remnant kidneys, an effect that is independent of TNa+; and thus 3) verapamil and phosphate restriction may slow progression of renal disease, at least in part by reducing renal metabolic demands.
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Tomasello, Sarah. "Anemia of Chronic Kidney Disease." Journal of Pharmacy Practice 21, no. 3 (June 2008): 181–95. http://dx.doi.org/10.1177/0897190008315906.
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Chronic kidney disease may result in complete kidney failure and contribute to many other health issues. Anemia is a logical consequence of the disease because the kidneys are the primary source of erythropoietin, the hormone that acts to stimulate red blood cell production in the bone marrow. All patients with chronic kidney disease are at risk for anemia, and treating anemia is extremely important to their health and well-being. Preventing or reversing the effects of anemia on the heart may decrease morbidity and mortality and improve quality of life. Many patients fail to receive treatment for anemia before requiring renal replacement therapy for end-stage renal disease. Pharmacists can play a vital role in screening, evaluating, designing proper treatment regimens, and monitoring patients with anemia of chronic kidney disease. Current recommendations regarding anemia are reviewed, including evaluation, pharmacotherapeutic agents, monitoring parameters, and goals of therapy.
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Lodh, Moushumi, Sandhya Lal, Binita Goswami, Partha Karmakar, and Ashok Kumar Parida. "Dyslipidemia in chronic renal failure: Cause or effect?" Asian Journal of Medical Sciences 7, no. 5 (August 31, 2016): 42–46. http://dx.doi.org/10.3126/ajms.v7i5.14755.
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Background: Various organ systems within the human body are intimately connected to each other. This organ crosstalk mediated by soluble & cellular mediators help maintain normal homeostasis & optimum body functioning. But during disease states, this very crosstalk can carry over the influence of the diseased organ to initiate & perpetuate functional dysfunctions in other organs. Chronic kidney disease may result from different conditions, which may be inherent to the kidney or a consequence of a systemic disease.Aims and Objectives: We conducted this study with the objective to study the metabolic abnormalities in chronic kidney disease patients admitted for dialysis. Such a study has not been documented earlier from this part of India.Materials and Methods: Milky serum of such patients has been recognized as early sign of dyslipidemia. We studied the lipid profile and mineral metabolism in chronic kidney disease and then reviewed all the biochemical pathways involved in etiopathogenesis of renal dyslipidemia.Results: Our study group showed significant hypocalcemia, hypermagnesemia, and hyperphosphatemia, hypoproteinemia, hypoalbuminemia and hyperglobulinemia. The lipid profile was also deranged with statistically significant elevation in total cholesterol and triglyceride levels and significantly lower HDL levels as compared to the controls.Conclusion: Such a study has not been documented earlier from eastern India. The metabolic abnormalities we have observed in chronic kidney disease enhance the risk of atherosclerotic cardiovascular disease in these patients. More prospective studies with larger sample size are required to establish the observations made in this study. Asian Journal of Medical Sciences Vol.7(5) 2016 42-46
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Memon, Shagufta, Navaid Kazi, Amin Fahim, Ghulam Shah Nizamani, and Anila Qureshi. "CHRONIC KIDNEY DISEASE." Professional Medical Journal 23, no. 07 (July 10, 2016): 784–88. http://dx.doi.org/10.29309/tpmj/2016.23.07.1639.
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Objectives: This study aimed to determine the platelet count in diagnosedchronic renal failure patients and to find out the association of platelet count with glomerularfiltration rate. Study Design: Case control study. Place of study: Diagnostic and researchlaboratory Liaquat University Hospital Hyderabad and Nephrology Unit, Isra University HospitalHyderabad. Duration of study: January 2015 to July 2015. Materials and methods: Total ofone hundred and twenty subjects (n=120) were divided into two groups. The healthy controls(n=60) were included in group-I whereas patients with chronic renal failure (n=60) were kept ingroup-II. 5 ml of blood was drawn and sent to laboratory for estimation of serum platelet count,blood urea nitrogen and serum creatinine levels. Results: The present study showed highlysignificant difference with marked decrease in the platelet counts seen in the CRF patientswith 223.9±89.1 million/μL in comparison to the 347.60±55.9 million/μl platelets in controlindividuals. Also the results of BUN in CRF patients showed highly significant differences with27.67±7.68 mg/dl when compared to controls having BUN 8.95±1.02 mg/dl. The comparisonbetween GFR with mean platelet count showed negative correlation (r = -0.27) in CRF patients.Conclusion: The present study shows weak negative correlation of platelet count with GFR.
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Díaz-Delgado, Oscar Bautista, and Briony Alderson. "Anaesthesia of the patient with chronic kidney disease." Companion Animal 25, no. 11 (December 2, 2020): 268–76. http://dx.doi.org/10.12968/coan.2020.0045.
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Chronic kidney disease is common, particularly in geriatric animals. General anaesthesia is usually required for routine procedures (dental prophylaxis, ovariohysterectomy or castration) and emergency procedures, which may have profound effects on the body, especially on cardiac output, subsequent blood pressure and on the perfusion of different vital organs. It is essential to understand the effects of renal dysfunction on the patient, as well as the effects that anaesthesia and surgery may have on the kidneys. The understanding of renal physiology, along with the effect of drug choices, is key to successful management of chronic renal failure.
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Tkachenko, L. A., U. A. Kostrikova, T. I. Yarmola, G. L. Pustovoit, and V. V. Talash. "KIDNEY DAMAGE IN PATIENTS WITH RHEUMATOID ARTHRITIS." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 19, no. 2 (July 19, 2019): 246–50. http://dx.doi.org/10.31718/2077-1096.19.2.246.
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The purpose of this work is to perform a general analysis of relevant literature on the issue of kidney damage in patients with rheumatoid arthritis. Kidney damage in patients with rheumatic diseases is potentially dangerous, as it can lead to the development of terminal renal failure that may require replacement renal therapy. Amyloidosis often leads to kidney failure in patients with rheumatoid arthritis. Renal amyloidosis more often develops in patients with acute course of rheumatoid arthritis and under maximal immunological disorders. In patients with renal amyloidosis against the background of rheumatoid arthritis, manifestations of joint affection decrease, while the renal-uremic syndrome takes a predominant role. Signs of nephrotic syndrome and chronic renal failure develop gradually. Kidney damage can be caused by medications for rheumatoid arthritis. The choice of the optimal scheme of individual-centred therapy is vitally important for patients, since every aggravation of both rheumatic disease and secondary renal damage leads to the progression of chronic renal failure.
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Rabrenovic, Violeta, Slobodan Culafic, Milorad Rabrenovic, Tamara Dragovic, Sasa Tresnjic, Sinisa Masic, Radomir Matunovic, et al. "Intracranial aneurysm as extra-renal manifestation of polycystic kidney disease: A case report." Vojnosanitetski pregled 75, no. 5 (2018): 525–30. http://dx.doi.org/10.2298/vsp160728020r.
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Introduction. Polycystic kidney disease is a hereditary kidney disease characterized by the occurrence of cysts (fluid-filled enlargements) in cortex or medula of the kidney, and is inherited in an autosomal dominant or autosomal recessive manner. In addition to multiple cysts in kidneys, there may be many extra-renal manifestations (cysts of the liver, pancreas, lungs, heart, etc.), among which the most serious one is intracranial aneurysms. Case report. A 57-year-old female patient with polycystic kidney disease and stage IV renal failure was hospitalized at our clinic due to decreased renal function, the development of urinary tract infections, headaches and unregulated blood pressure despite the usual treatment. This patient also had a number of associated diseases: obesity, diabetes mellitus (the insulindependent type), hypothyroidism, and depression syndrome. After better regulation of blood pressure, resolved urinary tract infections and improved renal function, there were still persistent headaches (resulting in the excessive use of analgesics). With adequate preparation, multislice computed tomography (MSCT) angiography of blood vessels of the head was performed. As a result, we diagnosed the saccular intracranial aneurysm (IA) with anterior localization. Regarding the symptoms, age and comorbidity, digital subtraction angiography (DSA) was performed, and showed saccular IA (5.2 mm ? 4 mm), with wide neck affecting both middle cerebral artery branches (MCA). During the procedure the stent was placed, which filled the aneurysm with spirals, cutting it off from circulation. After the successful procedure and without further complications, the patient no longer had headaches and blood pressure was maintained within the required limits with stable parameters of chronic renal failure. Conclusion. The case of the patient with polycystic kidney disease, stage IV chronic renal failure, with a number of comorbidities (headache, obesity, hypertension, diabetes mellitus, hypothyroidism) and diagnosed with symptomatic intracranial aneurysm was successfully solved with a multidisciplinary approach, emphasizing the importance of teamwork in daily practice.
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Yoder, Bradley K., Sharon Mulroy, Hannah Eustace, Catherine Boucher, and Richard Sandford. "Molecular pathogenesis of autosomal dominant polycystic kidney disease." Expert Reviews in Molecular Medicine 8, no. 2 (January 17, 2006): 1–22. http://dx.doi.org/10.1017/s1462399406010362.
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Autosomal dominant polycystic kidney disease (ADPKD) is one of the commonest inherited human disorders yet remains relatively unknown to the wider medical, scientific and public audience. ADPKD is characterised by the development of bilateral enlarged kidneys containing multiple fluid-filled cysts and is a leading cause of end-stage renal failure (ESRF). ADPKD is caused by mutations in two genes: PKD1 and PKD2. The protein products of the PKD genes, polycystin-1 and polycystin-2, form a calcium-regulated, calcium-permeable ion channel. The polycystin complex is implicated in regulation of the cell cycle via multiple signal transduction pathways as well as the mechanosensory function of the renal primary cilium, an enigmatic cellular organelle whose role in normal physiology is still poorly understood. Defects in cilial function are now documented in several other human diseases including autosomal recessive polycystic kidney disease, nephronophthisis, Bardet–Biedl syndrome and many animal models of polycystic kidney disease. Therapeutic trials in these animal models of polycystic kidney disease have identified several promising drugs that ameliorate disease severity. However, elucidation of the function of the polycystins and the primary cilium will have a major impact on our understanding of renal cystic diseases and will create exciting new opportunities for the design of disease-specific therapies.
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VOGLER, CAROLE, SHARON HOMAN, ALETHA PUNG, CONSTANCE THORPE, JANE BARKER, EDWARD H. BIRKENMEIER, and POORNIMA UPADHYA. "Clinical and Pathologic Findings in Two New Allelic Murine Models of Polycystic Kidney Disease." Journal of the American Society of Nephrology 10, no. 12 (December 1999): 2534–39. http://dx.doi.org/10.1681/asn.v10122534.
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Abstract. Patients with inherited cystic kidney diseases have progressive cystic dilation of nephrons with concomitant loss of functional renal parenchyma and renal failure. Animal models of inherited cystic kidney disease are useful for study of the pathogenesis and molecular basis of cystic renal diseases. This article describes the clinical and pathologic features in two spontaneously occurring murine models of inherited polycystic kidney disease due to independent allelic mutations on mouse chromosome 8. The mutations, designatedkatandkat2J, affect a chromosomal segment homologous to a region of human chromosome 4q35; the altered gene has not yet been identified. An allelism test showed that the mutations are at the same locus. The phenotype, inherited as an autosomal recessive, is more severe inkat2J/kat2Jmice. Their kidneys are morphologically normal at birth, but by 3 mo of age, cysts affect all levels of the nephron. Adult males have testicular hypoplasia and they are sterile. A few of the oldestkat2J/kat2Jmice have focal portal bile duct proliferation and dilation.kat2J/kat2Jmice develop anemia and uremia and die before 1 yr of age. Inkat/katmice, the renal cystic disease progresses more slowly but is morphologically similar to that ofkat2J/kat2Jmice. The progressive cystic transformation of the kidneys in these allelic murine models resembles that seen in humans with autosomal dominant polycystic kidney disease.
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Seravalle, Gino, Fosca Quarti-Trevano, Jennifer Vanoli, Chiara Lovati, and Guido Grassi. "Autonomic cardiovascular alterations as therapeutic targets in chronic kidney disease." Clinical Autonomic Research 31, no. 4 (February 19, 2021): 491–98. http://dx.doi.org/10.1007/s10286-021-00786-6.
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Abstract Purpose The present paper will review the impact of different therapeutic interventions on the autonomic dysfunction characterizing chronic renal failure. Methods We reviewed the results of the studies carried out in the last few years examining the effects of standard pharmacologic treatment, hemodialysis, kidney transplantation, renal nerve ablation and carotid baroreceptor stimulation on parasympathetic and sympathetic control of the cardiovascular system in patients with renal failure. Results Drugs acting on the renin–angiotensin system as well as central sympatholytic agents have been documented to improve autonomic cardiovascular control. This has also been shown for hemodialysis, although with more heterogeneous results related to the type of dialytic procedure adopted. Kidney transplantation, in contrast, particularly when performed together with the surgical removal of the native diseased kidneys, has been shown to cause profound sympathoinhibitory effects. Finally, a small amount of promising data are available on the potential favorable autonomic effects (particularly the sympathetic ones) of renal nerve ablation and carotid baroreceptor stimulation in chronic kidney disease. Conclusions Further studies are needed to clarify several aspects of the autonomic responses to therapeutic interventions in chronic renal disease. These include (1) the potential to normalize sympathetic activity in uremic patients by the various therapeutic approaches and (2) the definition of the degree of sympathetic deactivation to be achieved during treatment.
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Ware, Thuvaraka. "Chronic kidney disease." InnovAiT: Education and inspiration for general practice 11, no. 1 (January 2018): 35–40. http://dx.doi.org/10.1177/1755738017738272.
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Chronic kidney disease (CKD) is a broad term used to describe any abnormality of kidney structure or function. It is often asymptomatic in the early stages and co-exists with other chronic illnesses, such as diabetes and hypertension. It is associated with an increased risk of cardiovascular disease, end-stage renal failure, anaemia and metabolic bone disease. Early detection of CKD and managing risk factors may provide an opportunity to prevent progression of associated risks. This article will discuss the diagnosis, classification, management and complications of CKD, and when to refer to secondary care.
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Kelly, K. J. "Acute Renal Failure: Much More Than a Kidney Disease." Seminars in Nephrology 26, no. 2 (March 2006): 105–13. http://dx.doi.org/10.1016/j.semnephrol.2005.09.003.
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T, Schiavello, Burke V, Jasik P, Melsom S, Sulowicz W, Krasniak A, Stompor T, Kalaydjieva L, Thomas M, and Lim W. "SMOKING AND RENAL FAILURE IN POLYCYSTIC KIDNEY DISEASE (ADPKD)." Nephrology 7, no. 1 (February 2002): A147. http://dx.doi.org/10.1046/j.1440-1797.2002.00007-1-147.x.
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Liu, Yongmei, and Barry I. Freedman. "Genetics of progressive renal failure in diabetic kidney disease." Kidney International 68 (December 2005): S94—S97. http://dx.doi.org/10.1111/j.1523-1755.2005.09917.x.
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Koushik, Nikhil S., Steven F. McArthur, and Anne D. Baird. "Adult Chronic Kidney Disease: Neurocognition in Chronic Renal Failure." Neuropsychology Review 20, no. 1 (August 25, 2009): 33–51. http://dx.doi.org/10.1007/s11065-009-9110-5.
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Poptsov, V. N. "COMBINED HEART-KIDNEY TRANSPLANTATION." Russian Journal of Transplantology and Artificial Organs 18, no. 1 (April 16, 2016): 78–82. http://dx.doi.org/10.15825/1995-1191-2016-1-78-82.
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Combined heart-kidney transplantation may be performed in carefully selected patients with end-stage heart disease and renal failure. There are two types of combined transplantation of heart and kidney: 1) simultaneous heart-kidney transplantation (SHKT) from the same donor; 2) staged transplantation of heart and kidneys from two genetically different donors. The ISHLT registry in 2014 reported an increase in the number of SHKT over the years: from 22 in 1994 to 97 in 2012. World experience demonstrated excellent results of SHKT. Recipients of SHKT had superior survival, lower rates of acute cardiac and renal rejection compared to heart recipients. This article discusses the indications for simultaneous or staged heart-kidney transplantation in patients with dialysis-independent or dialysis-dependent renal failure, results and posttransplant survival of SHKT recipients. The author describes his own experience of 2 staged combined heart-kidney transplantations.
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Villegas, Iván, Edwin Quintero, Arnaldo Arrieta, Richard Leclercq, and Lyda Pérez. "Late-onset renal failure from angiotensin blockade in 51 chronic kidney disease patients." Revista Colombiana de Nefrología 3, no. 1 (January 1, 2016): 20–25. http://dx.doi.org/10.22265/acnef.3.1.237.
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Kurbegovic, Almira, and Marie Trudel. "Acute kidney injury induces hallmarks of polycystic kidney disease." American Journal of Physiology-Renal Physiology 311, no. 4 (October 1, 2016): F740—F751. http://dx.doi.org/10.1152/ajprenal.00167.2016.
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Acute kidney injury (AKI) and autosomal dominant polycystic kidney disease (ADPKD) are considered separate entities that both frequently cause renal failure. Since ADPKD appears to depend on a polycystin-1 (Pc1) or Pc2 dosage mechanism, we investigated whether slow progression of cystogenesis in two Pkd1 transgenic mouse models can be accelerated with moderate ischemia-reperfusion injury (IRI). Transient unilateral left ischemic kidneys in both nontransgenic and transgenic mice reproducibly develop tubular dilatations, cysts, and typical PKD cellular defects within 3 mo post-IRI. Similar onset and severity of IRI induced-cystogenesis independently of genotype revealed that IRI is sufficient to promote renal cyst formation; however, this response was not further amplified by the transgene in Pkd1 mouse models. The IRI nontransgenic and transgenic kidneys showed from 16 days post-IRI strikingly increased and sustained Pkd1/Pc1 (>3-fold) and Pc2 (>8-fold) expression that can individually be cystogenic in mice. In parallel, long-term and important stimulation of hypoxia-inducible factor 1α expression was induced as in polycystic kidney disease. While mammalian target of rapamycin signaling is activated, stimulation of the Wnt pathway, with markedly increased active β-catenin and c-Myc expression in IRI renal epithelium, uncovered a similar regulatory cystogenic response shared by IRI and ADPKD. Our study demonstrates that long-term AKI induces cystogenesis and cross talk with ADPKD Pc1/Pc2 pathogenic signaling.
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Throssell, D., J. Brown, K. P. G. Harris, and J. Walls. "Metabolic Acidosis Does Not Contribute to Chronic Renal Injury in the Rat." Clinical Science 89, no. 6 (December 1, 1995): 643–50. http://dx.doi.org/10.1042/cs0890643.
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1. Metabolic acidosis invariably accompanies chronic renal failure, and short periods of metabolic acidosis cause renal growth and proteinuria in normal rats. Rates of ammoniagenesis are increased in chronic renal failure, and it has been suggested that this contributes to disease progression. This study assessed (i) whether prolonged acidosis causes chronic renal injury in the normal kidney and (ii) whether abrogation of acidosis slows disease progression in the remnant kidney. 2. Metabolic acidosis was induced in normal rats by dietary hydrochloric acid. Urinary excretion of total protein, lysozyme and albumin increased, peaking at week 8 but returning to baseline by week 14. At killing after 14 weeks, kidney weights, glomerular filtration rates and serum creatinine were the same in both groups, but kidney/body weight and kidney/heart weight ratios were greater in the acidotic group. All kidneys were normal by light microscopy. 3. Rats subjected to five-sixths nephrectomy were given sufficient dietary bicarbonate to abolish uraemic acidosis, and their outcome was compared with that of non-alkalinized remnants (controls). Proteinuria, glomerular filtration rates, blood pressure, histological injury and time to the development of terminal uraemia were no better in bicarbonate-supplemented animals than in controls. 4. These data demonstrate that metabolic acidosis neither causes nor exacerbates chronic renal injury. We conclude that the treatment of uraemic acidosis is unlikely to influence disease progression in patients with chronic renal failure.
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Alkadomi, Sumia Abded Alhafeth, Najah Sami Shawish, Saiel Hayat Saleh, and Amani Mustafa Alqudah. "Spectrum and contributing factors of renal diseases among Jordanian children." Clinical Nursing Studies 7, no. 4 (November 29, 2019): 70. http://dx.doi.org/10.5430/cns.v7n4p70.
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Renal diseases are a significant cause of morbidity and mortality in children. They can affect children in various ways: they vary from completely treatable without long-lasting consequences to severe disorders such as chronic kidney disease. The causes of renal disease may differ from one country to another. Understanding the spectrum and identifying the contributing factors of renal diseases in a specific country promote early diagnosis, facilitate treatment, and prevent complications such as renal failure and end-stage kidney disease. This study was conducted to establish the spectrum and contributing factors to renal diseases among Jordanian children receiving health care in a tertiary hospital in Amman, Jordan (Prince Hamza Hospital). A convenience sample of 129 children diagnosed with renal diseases, treated and followed in our nephrology clinic, were interviewed during 2015 to 2017. A kidney-disease patient questionnaire was used to interview the children or their caregivers. The study revealed that the most common renal disease among the participants was urinary tract infection (UTI, 35.7%), followed by congenital diseases (34.1%), then chronic renal failure (CRF, 11.6%). There were several contributing factors of renal disease among the studied children, such as malnutrition, poverty, high rate of consanguinity, delayed diagnosis, and geographical location.
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Nasybullina, A. A., O. V. Bulashova, V. M. Gazizyanova, M. I. Malkova, E. E. Mustafin, and G. R. Khusnutdinova. "Markers of inflammation in patients with heart failure in association with chronic kidney disease." Kazan medical journal 97, no. 6 (December 15, 2016): 881–87. http://dx.doi.org/10.17750/kmj2016-881.
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Aim. Evaluation of markers of systemic inflammation in patients with chronic heart failure in comorbidity with chronic kidney disease.Methods. The study included 188 patients with heart failure and kidney disease including control group (76 patients) with heart failure with preserved renal function aged 38 to 83 years (mean age 66.8±10.1 years), with the duration of heart failure of about 8 years. Quantitative measurement of C-reactive protein and proteins of blood serum and daily excretion of protein with urine were performed.Results. Glomerular filtration rate in patients without renal pathology was 71.1±11.7 ml/min/1.73 m2, and in the group with heart failure associated with kidney dysfunction it was 51.5±19.1 ml/min/1.73 m2. C-reactive protein, γ-globulin, albumin and total serum protein in patients with chronic kidney disease differed from those in patients with heart failure without kidney damage.Conclusion. C-reactive protein and γ-globulin in the serum significantly increase in patients with heart failure and chronic kidney disease and can be used as markers of cardiac as well as renal events.
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Bagdasarova, I. V., and S. P. Fomina. "CHRONICKIDNEYDISEASE IN CHILDREN AND RENAL REPLACEMENT THERAPYIN UKRAINE." Ukrainian Journal of Nephrology and Dialysis, no. 1(45) (January 26, 2015): 3–7. http://dx.doi.org/10.31450/ukrjnd.1(45).2015.01.
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Classification of Chronic Kidney Disease and stages of Chronic Renal Failure in children were compared. There was presented adapted Schwartz formula for estimated Glomerular Filtration Rate. Prevalence of the genitourinary system diseases in Ukrainian children was considered. There was first time systematized data on Chronic Kidney Disease in children and renal replacement therapy in the years 2009-2014.
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Khubutiya, B. Z., O. N. Rzhevskaya, and A. A. Lisenok. "Current possibilities of improving the results of kidney transplantation in patients of the older age group, including those with an aggravated urological history." Transplantologiya. The Russian Journal of Transplantation 13, no. 2 (June 21, 2021): 165–78. http://dx.doi.org/10.23873/2074-0506-2021-13-2-165-178.
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Introduction. All over the world and in Russia, the number of patients requiring dialysis therapy and kidney transplantation for chronic renal failure in the end-stage of the renal disease is increasing. In many countries of the world, the number of dialysis patients over 60 years of age accounts for 30 to 45% of all patients with chronic renal failure. Meantime, taking into account the improved methods for early diagnosis of chronic renal failure and the treatment methods for chronic kidney disease, including the renal replacement therapy, we can expect an increase in the number of elderly potential kidney transplant recipients. The likelihood of receiving a renal graft in elderly patients is significantly lower than in young recipients. Elderly patients are known to have a higher risk of death while waiting for a kidney transplant due to higher morbidity and lethality on dialysis. For this reason, the urgency of increasing the availability of kidney transplantation in elderly patients is growing over time. One of the solutions can be the use of kidneys from suboptimal donors with a far from ideal graft quality, but which could meet the needs for transplant care of the older age group of patients. The older age of a recipient entails a certain risk of developing a graft dysfunction due to the presence of concomitant diseases, and the potential risk increases even more with kidney transplants from expanded criteria donors. If a reduced functional reserve of kidneys removed from donors with extended criteria is identified, two-kidney transplantation is possible, which provides fairly good long-term results. To reduce the risk of a kidney graft loss, a careful selection of recipients is necessary, taking into account their co-morbidities, including the presence of urological diseases that impair the function of the upper and lower urinary tract. Their timely identification and correction makes it possible to raise the availability of kidney transplantation for elderly patients and improve its results. This review presents the results of the studies conducted in various world transplant centers, covers the mortality rates, kidney graft and recipient survival rates.The study purpose was to summarize the actual data and the results of the study on kidney transplantation in elderly patients with urological pathology.
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Meyrier, A., and P. Simon. "Drooping upper eyelids and polycystic kidney disease." Journal of the American Society of Nephrology 5, no. 5 (November 1994): 1266–70. http://dx.doi.org/10.1681/asn.v551266.
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Over the last 26 yr, 33 cases and/or families of patients with autosomal dominant polycystic kidney disease (ADPKD) and a particular appearance of the eyes have been observed. ADPKD was unremarkable and in most cases had led to the usual slow development of end-stage renal failure. The facial feature concerned the upper eyelid, which drooped obliquely over the eyeball with a fold hiding the upper segment of the iris (blepharochalasis). The aspect was so typical that the diagnosis of ADPKD was suggested on first contact with new renal patients. All affected patients were white, of various origins, including French, Polish, Scandinavian, Italian, and Spanish. In retrospect, drooping eyelids had been present in the parents and/or grandparents who had died of renal failure, with or without an established diagnosis of ADPKD. In order to disclose the cosegregation of blepharochalasis with ADPKD, the screening of its prevalence in a well-circumscribed region with a catchment population of 410,000 was undertaken. The facial feature was found in 24 (32%) of 75 ADPKD families. Family transmission was confirmed in those kindreds, because at least two members suffered from ADPKD. Cosegregation was sought by analyzing family group photographs taken over several generations, the oldest member of which was born in 1973. All members with blepharochalasis had died of renal failure or are presently being followed up for ADPKD. A bibliographic search showed that the association of ocular and/or eyelid deformities and various inborn renal diseases is far from rare, suggesting a simultaneous event in the embryonic timetable.(ABSTRACT TRUNCATED AT 250 WORDS)
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Wang, Hongting, Zuan-tao Lin, Yulin Yuan, and Tianfu Wu. "Urine biomarkers in renal allograft." Journal of Translational Internal Medicine 4, no. 3 (September 1, 2016): 109–13. http://dx.doi.org/10.1515/jtim-2016-0032.
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Abstract There is a high risk for the survival of patients with an end-stage renal disease for kidney transplantation. To avoid rejection by strict medication adherence is of utmost importance to avoid the failure of a kidney transplant. It is imperative to develop non-invasive biomarkers to assess immunity risk, and to ultimately provide guidance for therapeutic decision-making following kidney transplantation. Urine biomarkers may represent the promising non-invasive tools that will help in predicting risk or success rates of kidney transplantations. Furthermore, composite urinary biomarkers or urinary biomarker panel array might be critical in improving the sensitivity and specificity in reflecting various risks of kidney failure during transplantation. This review primarily focuses on the role of such biomarkers in predicting chronic kidney disease (CKD) progression and/or cardiovascular disease (CVD) risk in renal allograft.
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Alelign, Tilahun, and Beyene Petros. "Kidney Stone Disease: An Update on Current Concepts." Advances in Urology 2018 (2018): 1–12. http://dx.doi.org/10.1155/2018/3068365.
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Kidney stone disease is a crystal concretion formed usually within the kidneys. It is an increasing urological disorder of human health, affecting about 12% of the world population. It has been associated with an increased risk of end-stage renal failure. The etiology of kidney stone is multifactorial. The most common type of kidney stone is calcium oxalate formed at Randall’s plaque on the renal papillary surfaces. The mechanism of stone formation is a complex process which results from several physicochemical events including supersaturation, nucleation, growth, aggregation, and retention of urinary stone constituents within tubular cells. These steps are modulated by an imbalance between factors that promote or inhibit urinary crystallization. It is also noted that cellular injury promotes retention of particles on renal papillary surfaces. The exposure of renal epithelial cells to oxalate causes a signaling cascade which leads to apoptosis by p38 mitogen-activated protein kinase pathways. Currently, there is no satisfactory drug to cure and/or prevent kidney stone recurrences. Thus, further understanding of the pathophysiology of kidney stone formation is a research area to manage urolithiasis using new drugs. Therefore, this review has intended to provide a compiled up-to-date information on kidney stone etiology, pathogenesis, and prevention approaches.
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de Oliveira, Patrick, Kaile Cunha, Precil Neves, Monique Muniz, Giuseppe Gatto, Natalino Salgado Filho, Felipe Guedes, and Gyl Silva. "Renal Morphology in Coronavirus Disease: A Literature Review." Medicina 57, no. 3 (March 11, 2021): 258. http://dx.doi.org/10.3390/medicina57030258.
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Renal biopsy is useful to better understand the histological pattern of a lesion (glomerular, tubulointerstitial, and vascular) and the pathogenesis that leads to kidney failure. The potential impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on the kidneys is still undetermined, and a variety of lesions are seen in the kidney tissue of coronavirus disease patients. This review is based on the morphological findings of patients described in case reports and a series of published cases. A search was conducted on MEDLINE and PubMed of case reports and case series of lesions in the presence of non-critical infection by SARS-CoV-2 published until 15/09/2020. We highlight the potential of the virus directly influencing the damage or the innate and adaptive immune response activating cytokine and procoagulant cascades, in addition to the genetic component triggering glomerular diseases, mainly collapsing focal segmental glomerulosclerosis, tubulointerstitial, and even vascular diseases. Kidney lesions caused by SARS-CoV-2 are frequent and have an impact on morbidity and mortality; thus, studies are needed to assess the morphological kidney changes and their mechanisms and may help define their spectrum and immediate or long-term impact.
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Zeier, Martin, Peter Fehrenbach, Steffen Geberth, Klaus Möhring, Rüdiger Waldherr, and Eberhard Ritz. "Renal histology in polycystic kidney disease with incipient and advanced renal failure." Kidney International 42, no. 5 (November 1992): 1259–65. http://dx.doi.org/10.1038/ki.1992.413.
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Okamoto, Ryuji, Yusuf Ali, Ryotaro Hashizume, Noboru Suzuki, and Masaaki Ito. "BNP as a Major Player in the Heart-Kidney Connection." International Journal of Molecular Sciences 20, no. 14 (July 22, 2019): 3581. http://dx.doi.org/10.3390/ijms20143581.
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Brain natriuretic peptide (BNP) is an important biomarker for patients with heart failure, hypertension and cardiac hypertrophy. Although it is known that BNP levels are relatively higher in patients with chronic kidney disease and no heart disease, the mechanism remains unknown. Here, we review the functions and the roles of BNP in the heart-kidney interaction. In addition, we discuss the relevant molecular mechanisms that suggest BNP is protective against chronic kidney diseases and heart failure, especially in terms of the counterparts of the renin-angiotensin-aldosterone system (RAAS). The renal medulla has been reported to express depressor substances. The extract of the papillary tips from kidneys may induce the expression and secretion of BNP from cardiomyocytes. A better understanding of these processes will help accelerate pharmacological treatments for heart-kidney disease.
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Murkamilov, I. T., I. S. Sabirov, Zh A. Murkamilova, V. V. Fomin, A. I. Sabirova, K. A. Aitbaev, B. Zh Imanov, N. A. Redzhapova, and F. A. Yusupov. "STRATIFICATION OF NEPHROCEREBRAL AND CARDIOVASCULAR RISK IN CHRONIC GLOMERULONEPHRITIS (LITERATURE REVIEW)." Russian Archives of Internal Medicine 8, no. 6 (December 3, 2018): 418–23. http://dx.doi.org/10.20514/2226-6704-2018-8-6-418-423.
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This article analyzes the literature data concerning the origin and progression of cerebrovascular and cardiac diseases in renal dysfunction. Cardiovascular diseases and chronic kidney disease have common “traditional” risk factors, while the population growth in patients with renal impairment is currently mainly due to secondary renal damage in socially important diseases such as obesity, hypertension, atherosclerosis, type 2 diabetes, ischemic heart disease and chronic heart failure. The presented data of scientific researches testify to the direct correlation correlation between the decrease of the renal function and the increased risk of cardioand cerebrovascular diseases and death, irrespective of other risk factors. Obesity and associated biological substrates are independent risk factors for persistent impairment of kidney function and an increase in the body mass index causes direct damage to the kidneys, due to the disrupted synthesis of fat cytokines by various cytokines with nephrotoxic action, and also mediated — by inducing the development of diabetes mellitus 2 type and arterial hypertension, which are the most frequent risk factors for chronic kidney disease and cardiovascular diseases. The presented data on the role of endothelial dysfunction in impaired renal function, which contributes to the formation of atherosclerosis, and the increase in the severity of the atherosclerotic process contributes to an increase in the sever ity of renal failure. Literature data on the value of the heart rate are also presented. The increase in the heart rate can lead to atherosclerotic densification of the arteries, which is associated with an increase in the rate of spread of the pulse wave with a violation of the mechanisms of autoregulation of the blood flow in the brain and kidneys.
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Omar, Sabry, and Ahmed Zedan. "Cardiorenal syndrome." Southwest Respiratory and Critical Care Chronicles 1, no. 1 (January 30, 2013): 11. http://dx.doi.org/10.12746/swrccc.v1i1.24.
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Cardiovascular disease is the leading cause of death in patients with chronic kidney disease. Heart failure may lead to acute kidney injury and vice versa. Chronic kidney disease may affect the clinical outcomes in patients with cardiovascular disorders. Renal impairment with any degree of albuminuria has been increasingly recognized as an independent risk factor for cardiovascular events and heart failure hospitalizations, while chronic heart failure may cause chronic kidney disease. The bidirectional nature of these disorders contributes to the complexity and the composite definitions of cardiorenal syndromes. However, the most important clinical trials in heart failure tend to exclude patients with significant renal dysfunction. The mechanisms whereby renal insufficiency worsens the outcome in heart failure are not known, and several pathways could contribute to the ‘‘vicious heart/kidney circle.’’ Traditionally, renal impairment has been attributed to the renal hypoperfusion due to reduced cardiac output and decreased systemic pressure. The hypovolemia leads to sympathetic activity, increased renin-angiotensin aldosterone pathway, and arginine-vasopressin release. These mechanisms cause fluid and sodium retention, peripheral vasoconstriction, and volume overload. Therapy to improve renal dysfunction, reduce neurohormonal activation and ameliorate renal blood flow could lead to a reduction in mortality and hospitalization in patients with cardiorenal syndrome.
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Colliou, Eloïse, Arnaud Del Bello, David Milongo, Fabrice Muscari, Marion Vallet, Ivan Tack, and Nassim Kamar. "Kidney Failure after Liver Transplantation." Transplantology 2, no. 3 (August 30, 2021): 315–35. http://dx.doi.org/10.3390/transplantology2030032.
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One-third of patients with cirrhosis present kidney failure (AKI and CKD). It has multifactorial causes and a harmful effect on morbidity and mortality before and after liver transplantation. Kidney function does not improve in all patients after liver transplantation, and liver transplant recipients are at a high risk of developing chronic kidney disease. The causes of renal dysfunction can be divided into three groups: pre-operative, perioperative and post-operative factors. To date, there is no consensus on the modality to evaluate the risk of chronic kidney disease after liver transplantation, or for its prevention. In this narrative review, we describe the outcome of kidney function after liver transplantation, and the prognostic factors of chronic kidney disease in order to establish a risk categorization for each patient. Furthermore, we discuss therapeutic options to prevent kidney dysfunction in this context, and highlight the indications of combined liver–kidney transplantation.
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Pljesa, Steva. "Autosomal dominant polycystic kidney disease." Srpski arhiv za celokupno lekarstvo 136, Suppl. 4 (2008): 340–47. http://dx.doi.org/10.2298/sarh08s4340p.
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Autosomal dominant polycystic kiney disease is a hereditary systemic disorder, characterized by the developement of cysts, mainly in the kidney and liver, also with gastrointestinal and cardiovascular abnormalities. It affects 4 to 6 million people wordwide and accounts for end-stage renal disease in 7-10% of dialysis patients. The genetic penetrance is 100%, all affected individuals develop renal cysts until 70 years of age, and because of a great renal function reserve only about 50% of patients develop some degree of renal failure until the age of 60. Autosomal dominant polycystic kiney disease is a heterogeneous disorder, from a clinical as well as from a genetic point of view. There are at least three genes responsible for the disease: PKD-1 gene localized on chromosome 16p in the 16p13.3 segment which encodes Polycystin 1 protein similar to membrane receptor, PKD-2 gene localized on chromosome 4q in 4q13-23 segment which encodes Polycystin 2 protein wery similar to voltage L type Ca++ channel as well as Na+ channel and PKD-3 gene of unknown localization. Specific proteins participate in regulation od cell proliferation, apoptosis, secretion, polarity, cell-matrix interactions as cell-cell interactions and lead to the developement of cystic kidney disease. Renal manifestations of disease include structural (cyst development), functional (concentration alility falls), endocrine (renin erythropoietin) abnormalities and extra- renal manifestations. A routine diagnostic methods are good case-history about cystic kidney disease in family, ultrasonographic examination of kidneys and computerized tomography. In therapy of autosomal dominant polycystic kiney disease, low protein diets may help, treatment of arterial hypertension with ACE inhibitors and angiotensin II receptor blockers, the vasopressin V2 antagonists (VSR), rapamycin and long-acting somatostatin analogue may have some benefit.
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Hazra, Anup, Richard Siderits, Cheryl Rimmer, and Noah Rolleri. "Autopsy Report with Clinical and Pathophysiologic Discussion of Autosomal Dominant Adult Polycystic Kidney Disease." Case Reports in Urology 2014 (2014): 1–3. http://dx.doi.org/10.1155/2014/727580.
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The average weight of a kidney is approximately 135 gm, measuring on average 10 × 6 × 4 cm. In hereditary conditions, autosomal dominant and autosomal recessive polycystic kidney disease, the shape, size, and the weight can be significantly abnormal, causing progressive renal failure, often necessitating dialysis or renal transplant for survival. We report a case of adult polycystic kidney disease in a 50-year-old female without a family history, who died of complications of the disease which included accelerated hypertension, and renal and cardiac failure.
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Geiger, Kyle, and Henry Mroch. "Limited Treatment Options in Primary Hyperoxaluria with Renal Failure." Case Reports in Nephrology and Dialysis 10, no. 3 (October 5, 2020): 104–8. http://dx.doi.org/10.1159/000510143.
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Primary hyperoxaluria (PH) is a rare autosomal recessive metabolic disorder where serum oxalate levels rise due to overproduction. The kidney tubule is a main target for oxalate deposition, resulting in damage to the organ. Kidney failure is rare in these patients. We present a 67-year-old female with hemodialysis-dependent end-stage renal disease likely due to PH type 2 or 3. With extremely high levels of serum oxalate (60.4 μmol/L), this patient had minimal treatment options for her rare disease. This report details a unique presentation of a rare disease where kidney biopsy was instrumental.
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Salas, Paulina, Viola Pinto, Josefina Rodriguez, Maria Jose Zambrano, and Veronica Mericq. "Growth Retardation in Children with Kidney Disease." International Journal of Endocrinology 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/970946.
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Growth failure is almost inextricably linked with chronic kidney disease (CKD) and end-stage renal disease (ESRD). Growth failure in CKD has been associated with both increased morbidity and mortality. Growth failure in the setting of kidney disease is multifactorial and is related to poor nutritional status as well as comorbidities, such as anemia, bone and mineral disorders, and alterations in hormonal responses, as well as to aspects of treatment such as steroid exposure. This review covers updated management of growth failure in these children including adequate nutrition, treatment of metabolic alterations, and early administration of recombinant human growth hormone (GH).
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Lai, S., A. Sciarra, F. Pierella, S. Pastore, L. Piloni, S. Salciccia, A. M. Perrotta, et al. "Chronic Kidney Disease and Urological Disorders: An Overview." Current Signal Transduction Therapy 15, no. 2 (December 1, 2020): 223–31. http://dx.doi.org/10.2174/1574362413666180412142930.
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Introduction: Chronic Kidney Disease (CKD) is a highly prevalent condition and it is a major risk factor for End-Stage Renal Disease (ESRD), cardiovascular disease, and premature death. Some congenital and acquired anomalies of the kidneys and lower urinary tract (CAKUT and CALUT) are well-known causes of CKD and ESRD, but often remain undiagnosed and their prevalence is underestimated. This study aims to provide an overview that considered mainly some of the major congenital and acquired urological diseases that could lead to renal clinical manifestations common even to the most widespread renal pathologies, for which often underdiagnosed. Materials and Methods: PubMed search was conducted for available English literature describing the actual knowledge on congenital and acquired urological disorders determining acute and chronic kidney disease. Prospective and retrospective studies as well as meta-analyses and latest systematic reviews were included. Results: Most of the studies examined and reviewed were discarded for wrong population or intervention or deemed unfit, and only 87 met the inclusion criteria for the review. The studies included in the review related to urological disorders that may determine chronic and acute kidney disease. Conclusion: Some urological diseases, as CAKUT and CALUT, especially in adults, show symptoms, as renal failure, proteinuria and hypertension, very common to other kidney diseases, for this reason may remain undiagnosed and their prevalence is not completely known. Therefore, in doubtful cases, non-invasive and inexpensive tests, as cystourethrogram, should be made, to rule out urological disorders and if necessary, ultrasonography, urography and scintigraphy, might allow a correct and early diagnosis of these defects and thus adequate therapy, preventing or at least slowing down an evolution toward CKD and ESRD.
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Stevanovic, Radmila, Sofija Glumac, Jovanka Trifunovic, Biljana Medjo, Tijana Nastasovic, and Jasmina Markovic-Lipkovski. "Autosomal recessive polycystic kidney disease: Case report." Srpski arhiv za celokupno lekarstvo 137, no. 5-6 (2009): 288–91. http://dx.doi.org/10.2298/sarh0906288s.
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Introduction. Autosomal recessive polycystic kidney disease is the most common heritable cystic renal disease occurring in infancy and childhood. The clinical spectrum of signs and symptoms of this disease is widely variable ranging from perinatal death to a milder progressive form, which cannot be diagnosed until adolescence. Case Outline. A female neonate born in the 35th/36th week of gestation. The findings of all standard medical examinations of the neonate done by the mother were within normal limits. A few days before delivery physicians at a regional medical centre revealed enlarged kidneys and oligohydramnios. The delivery was performed by caesarean section. The vital functions of the newborn were in critical condition so that she was referred to the University Children's Hospital in Belgrade. Soon after admission, despite all undertaken measures, the infant died. Autopsy was done at the Institute of Pathology of the Belgrade Clinical Centre. All findings were typical for autosomal recessive polycystic kidney disease. The kidneys were hugely enlarged, with cystically dilated collecting ducts that almost completely replaced the renal parenchyma. The lungs were mildly hypoplastic. The liver showed dilated portal spaces, with multiple irregularly branching bile ducts. The cause of death was respiratory distress and renal failure. Conclusion. In all cases of congenital anomalies of the kidney with lethal ending it is necessary to perform autopsy and aimed genetic investigation.
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Elsayed, Ata Sedik, Azab Elsayed Azab, and Nargis Omar Eaboda. "CORRELATION BETWEEN CHRONIC KIDNEY DISEASES AND HEMATOLGICAL DATA IN SABRATHA HOSPITAL IN LIBYA." Asian Journal of Pharmaceutical and Clinical Research 10, no. 2 (February 1, 2017): 291. http://dx.doi.org/10.22159/ajpcr.2017.v10i2.15595.
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In chronic kidney failure, there is impairment in the excretion of toxic non-volatile solutes, with consequent increase in the plasma concentrations of all metabolites derived mainly from protein metabolism, characterized by increased urea and creatinine, the prevalence and severity of anemia are related to the kidney disease stage and the relative deficiency or reduction in erythropoietin production is the main cause. This study aimed at checking the correlation between anemia and chronic kidney diseases in patients who underwent hemodialysis in Sabratha Hospital in the West of Libya. This study was conducted on 60 patients (36 males and 24 females) with chronic renal failure from October 2015 to April 2016 and a group of 40 (20 males and 20 females) individuals as control. The results of the study concluded that there is a correlation between progression of chronic kidney diseases and reduction in hemoglobin, red blood cells count, hematocrit, and serum iron.Keywords: Chronic kidney diseases, Chronic kidney disease, Anemia, Renal failure