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Liao, Hung-Wei, Shuo-Meng Wang, Chieh-Kai Chan, et al. "Transtubular potassium gradient predicts kidney function impairment after adrenalectomy in primary aldosteronism." Therapeutic Advances in Chronic Disease 11 (January 2020): 204062232094479. http://dx.doi.org/10.1177/2040622320944792.
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Background: In primary aldosteronism (PA), kidney function impairment could be concealed by relative hyperfiltration and emerge after adrenalectomy. We hypothesized transtubular gradient potassium gradient (TTKG), a kidney aldosterone bioactivity indicator, could correlate to end organ damage and forecast kidney function impairment after adrenalectomy. Methods: In the present prospective study, we enrolled lateralized PA patients who underwent adrenalectomy and were followed up 12 months after operation in the Taiwan Primary Aldosteronism Investigation (TAIPAI) registry from 2010 to 2018. The clinical outcome was kidney function impairment, defined as estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m2 at 12 months after adrenalectomy. End organ damage is determined by microalbuminuria and left ventricular mass. Results: In total, 323 patients [mean, 50.8 ± 10.9 years old; female 178 (55.1%)] were enrolled. Comparing pre-operation and post-operation data, systolic blood pressure, serum aldosterone, urinary albumin to creatinine ratio and eGFR decreased. TTKG ⩾ 4.9 correlated with pre-operative urinary albumin to creatinine ratio >50 mg/g [odds ratio (OR) = 2.42; p = 0.034] and left ventricular mass (B = 20.10; p = 0.018). Multivariate logistic regression analysis demonstrated that TTKG ⩾ 4.9 could predict concealed chronic kidney disease (OR = 5.42; p = 0.011) and clinical success (OR = 2.90, p = 0.017) at 12 months after adrenalectomy. Conclusions: TTKG could predict concealed kidney function impairment and cure of hypertension in PA patients after adrenalectomy. TTKG more than 4.9 as an adverse surrogate of aldosterone and hypokalaemia correlated with pre-operative end organ damage in terms of high proteinuria and cardiac hypertrophy.
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West, M. L., H. Sonnenberg, A. Veress, and M. L. Halperin. "The relationship between the plasma potassium concentration and renal potassium excretion in the adrenalectomized rat." Clinical Science 72, no. 5 (1987): 577–83. http://dx.doi.org/10.1042/cs0720577.
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1. The purpose of this study was to evaluate the renal mechanisms which lead to a high urine [K+] in adrenalectomized (ADX) rats devoid of aldosterone. 2. By dividing the urine [K+] by the urine to plasma osmolality ratio, the [K+] in the cortical collecting duct luminal fluid can be estimated; dividing this value by the plasma [K+] yields an index of the transtubular [K+] gradient (TTKG) in vivo. 3. The TTKG was close to 7 in aldosterone deficient ADX rats while on a normal K+ diet and fell towards unity when amiloride or a low K+ diet was administered to these rats. 4. With a longer time on a low K+ diet, the TTKG was less than 1 in ADX rats. This suggests that K+ was reabsorbed in the medullary collecting duct under these conditions. 5. Hyperkalemia appears to have an ‘aldosterone-like’ action in the cortical collecting duct in vivo in the absence of aldosterone in ADX rats. This action of hyperkalemia permits normal K+ excretion rates despite the absence of mineralocorticoids.
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Weinstein, Alan M. "A mathematical model of rat cortical collecting duct: determinants of the transtubular potassium gradient." American Journal of Physiology-Renal Physiology 280, no. 6 (2001): F1072—F1092. http://dx.doi.org/10.1152/ajprenal.2001.280.6.f1072.
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In assessing disorders of potassium excretion, urine composition is used to calculate the transtubular gradient (TTKG), as an estimate of tubule fluid concentration, at a point when the fluid was last isotonic to plasma, namely, within the cortical collecting duct (CCD). A mathematical model of the CCD has been developed, consisting of principal cells and α- and β-intercalated cells, and which includes Na+, K+, Cl−, HCO[Formula: see text], CO2, H2CO3, phosphate, ammonia, and urea. Parameters have been selected to achieve fluxes and permeabilities compatible with data obtained from perfusion studies of rat CCD under the influence of both antidiuretic hormone and mineralocorticoid. Both epithelial (flat sheet) and tubule models have been configured, and model calculations have focused on the determinants of the TTKG. Using the epithelial model, luminal K+ concentrations can be computed at which K+secretion ceases (0-flux equilibrium), and this luminal concentration derives from the magnitude of principal cell peritubular uptake of K+ via the Na-K-ATPase, relative to principal cell peritubular membrane K+ permeability. When the model is configured as a tubule and examined in the context of conditions in vivo, osmotic equilibration of luminal fluid produces a doubling of the initial K+ concentration, which, depending on delivered load, may be substantially greater than the zero-flux equilibrium value. Under such circumstances, the CCD will be a site for K+ reabsorption, although the relatively low permeability ensures that this reabsorptive flux is likely to be small. Osmotic equilibration may also raise luminal NH3 concentrations well above those in cortical blood. In this situation, diffusive reabsorption of NH3 provides a mechanism for base reclamation without the metabolic cost of active proton secretion.
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Supriyani, Yayik, Deka Viotra, and Putri Deas Hadilofyani. "Bartter Syndrome: A Case Report." Bioscientia Medicina : Journal of Biomedicine and Translational Research 7, no. 7 (2023): 3453–56. http://dx.doi.org/10.37275/bsm.v7i7.844.
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Background: Bartter's syndrome refers to a group of genetic disorders that affect the renal tubular system, which is responsible for reabsorbing various substances such as sodium, potassium, and chloride from the urine into the blood. This study aimed to present a clinical case related to Bartter syndrome.
 Case presentation: A 52-year-old male patient in the internal medicine department of Dr. M. Djamil General Hospital Padang with the main complaint of weakness in both legs increasing since 1 day ago. On laboratory examination, the patient found potassium 1.7 mmol/L, indicating hypokalemia. Renal function examination showed normal kidney function. Examination of blood gas analysis showed results of metabolic alkalosis. Examination of urine potassium obtained potassium levels of 22 mmol/day, urine osmolarity of 140 mOsm/kgH2O at serum osmolarity of 274 mOsm/kgH2O, with TTKG (transtubular potassium gradient) = 28. The patient was diagnosed with Bartter syndrome. Treatment is carried out by administering KSR tablets 3x600 mg orally while monitoring electrolytes regularly.
 Conclusion: This patient has hypokalemia, metabolic alkalosis, normal magnesium and calcium, and hypercalciuria. This patient is diagnosed with Bartter syndrome.
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Sakaguchi, Taiki, Kazuya Shinouchi, Hiroyuki Miura, et al. "Transtubular Potassium Gradient (TTKG) as a Surrogate for Monitoring Aldosterone Bioactivity in Patients with Acute Decompensated Heart Failure." Journal of Cardiac Failure 20, no. 10 (2014): S181—S182. http://dx.doi.org/10.1016/j.cardfail.2014.07.282.
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Kim, Yeo-Kyeoung, Soo-Young Bae, Li Yu, et al. "Renal Adverse Effect of Anagrelide in Patients with Myeloproliferative Neoplasms." Blood 118, no. 21 (2011): 5151. http://dx.doi.org/10.1182/blood.v118.21.5151.5151.
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Abstract Abstract 5151 Background: Along with hydroxyurea, anagrelide has been widely used for the treatment of myeloproliferative neoplasms (MPNs). In contrast to hydroxyurea, anagrelide selectively inhibits megakaryocyte colony development and its cytoreductive effect relatively limited to platelets, hence, it usually used as a first line therapy for the patients with essential thrombocytosis (ET). The frequently reported adverse events of anagrelide are palpitation, headache, edema, and vague abdominal symptoms. Renal insufficiency as a complication of anagrelide treamtent is not well recognized. Some studies suggested that anagrelide has a possible relationship to renal failure, especially in the patients with preexisting renal diseases. A few cases of acute interstitial nephritis or renal tubular necrosis were reported sporadically. However, the relationship between anagrelide and renal insufficiency remain unclear, and its mechanism remains to be further elucidated. In the present study, we investigated the incidence and the characteristics of renal impairment in anagrelide-treated patients with MPNs. Methods: Total 335 patients with thrombocythemia due to MPNs who showed normal renal function before starting treatment were enrolled. They were serially assessed renal function and serum potassium levels. Treatment modalities such as anagrelide, hydroxyurea, phlebotomy or combination were decided by the characteristics of presenting cytosis and patients' tolerability. If the patients showed renal impairment during the treatment period, other parameters such as co-morbidities, combined medication history, electrolytes imbalance, urine analysis, and imaging studies were fully assessed in order to find the existing causes of renal failure. Results: Of total enrolled 335 patients, 54.0% with ET, 33.4% with polycythemia vera (PV), 3.3% with primary myelofibrosis, 0.6% with chronic neutrophilic leukemia (CNL), and 6.6% with MPN, unclassifiable. Others were diseases categorized as a myelodysplastic (MDS)/MPN (1.5% with atypical chronic myeloid leukemia and 0.6% with chronic myelomonocytic leukemia). In terms of treatment modalities, 56.7% were anagrelide group (anagrelide alone, anagrelide+hydroxyurea, and anagrelide+phlebotomy), whereas 43.3% were non-anagrelide group (hydroxyurea alone and hydroxyurea+phlebotomy). The median age of anagrelide group was 61 years (ranges; 19–84 years) and non-anagrelide group was 57 years (ranges: 14–84 years). In anagrelide group, the median serum creatinine levels before starting treatment was 0.8 mg/dL (ranges: 0.5–1.3 mg/dL). In non-anagrelide group, median serum creatinine was 0.9 mg/dL (ranges: 0.4–1.3 mg/dL). After addressing the treatment, forty-six (24.2%) in anagrelide group revealed increases of serum creatinine (median: 1.5 mg/dL, ranges: 1.4–2.3) above the normal reference ranges. Median estimated glomerular filtration rate (eGFR) using the Modification of Diet in Renal Disease (MDRD) equation in these patients was 39.5 mL/min/1.73 m2 (ranges; 21.0–56.0). On the other hand, in non-anagrelide group, only 7.6% showed increases of serum creatinine (median 1.5 mg/dL, ranges: 1.4–2.0) and decreases of eGFR (median; 43 mL/min/1.73 m2, ranges: 32–53) (P=0.000). The relative risk ratio (RR) for renal impairment of anagrelide use was 3.89 (C.I.: 1.94–7.83) (P=0.000). Median time to develop renal impairment from the start of anagrelide was 13.8 months (ranges; 0.2–53.4 months). In anagrelide group, 8.4% have diagnosed as diabetes mellitus (DM) before starting the anagrelide, however, the preexisting DM was not significantly related to the development of renal failure (RR=1.26, P=0.649). Of total 46 patients who showed renal impairment after anagrelide use, mild to moderate proteinuria (grade 1 or 2) were revealed in ten patients (21.7%). Furthermore, nine patients (19.6%) showed the features of hyperkalemic renal tubular acidosis which was charaterized by metabolic acidosis, hyperkalemia, and low transtubular potassium gradient (TTKG < 5). Conclusions: In the present study, we suggested the possible casual relationship between anagrelide therapy and renal impairment. Although large randomized studies and more detailed analyses to find the underlying mechianisms may be warranted, caution and serial follow-up of renal function should be indicated in MPN patients with anagrelide treatment. Disclosures: No relevant conflicts of interest to declare.
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Kamel, K. S., J. H. Ethier, S. Quaggin, et al. "Studies to determine the basis for hyperkalemia in recipients of a renal transplant who are treated with cyclosporine." Journal of the American Society of Nephrology 2, no. 8 (1992): 1279–84. http://dx.doi.org/10.1681/asn.v281279.
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Hyperkalemia is commonly encountered in patients who receive a renal transplant and the immunosuppressive drug, cyclosporine. There is also a high incidence of hypertension (which is thought to be due to expansion of the extracellular fluid volume) and hyperchloremic metabolic acidosis in this group of patients. This constellation of findings led to the suspicion of the possibility that their basis might be type II hypoaldosteronism. To test this hypothesis, 12 patients with hyperkalemia (plasma K+, 5.1 +/- 0.2 mmol/L at the time of study) while receiving cyclosporine were studied. Patients who had diabetes mellitus, those receiving drugs known to cause hyperkalemia (e.g., beta blockers, angiotensin-converting enzyme inhibitors, K(+)-sparing diuretics), or those with a serum creatinine greater than 200 mumol/L were excluded. The renal response to hyperkalemia was inappropriate because the transtubular K+ concentration gradient (TTKG) was only 4.3 +/- 0.4 compared with a TTKG of 13 +/- 1, 2 h after 50 mmol of KCl was given to normal subjects. The TTKG, after administration of 200 micrograms of fludrocortisone, was still very low (5.6 +/- 0.6) in the patients compared with that of controls (12 +/- 1). After administration of 250 to 500 mg of acetazolamide to increase the delivery of bicarbonate to the distal nephron, the TTKG rose significantly to 11 +/- 1 in patients on cyclosporine, compared with 17 +/- 1 in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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Tan, Jia Wei, Kwabena S. Nketiah Sarpong, Sun-Joo Jang, Samdish Sethi, Lakshmi D. Polisetty, and Arjun Gogna. "Transtubular Potassium Gradient in Hypertensive Emergency." Journal of the American Society of Nephrology 33, no. 11S (2022): 931. http://dx.doi.org/10.1681/asn.20223311s1931b.
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Nako, Y., Yasushi Ohki, Akira Harigaya, Takeshi Tomomasa, and Akihiro Morikawa. "Transtubular potassium concentration gradient in preterm neonates." Pediatric Nephrology 13, no. 9 (1999): 880–85. http://dx.doi.org/10.1007/s004670050720.
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Dom�nguez, Pedro, Francisco Castell�, Guillem Pintos, et al. "Some questions about the transtubular potassium concentration gradient." Pediatric Nephrology 5, no. 1 (1991): 94–95. http://dx.doi.org/10.1007/bf00852856.
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Wilson, Rod W., Mark Wareing, Jon Kibble, and Roger Green. "Potassium permeability in the absence of fluid reabsorption in proximal tubule of the anesthetized rat." American Journal of Physiology-Renal Physiology 274, no. 6 (1998): F1109—F1112. http://dx.doi.org/10.1152/ajprenal.1998.274.6.f1109.
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A luminal microperfusion technique was used to examine the K+ permeability of surface proximal convoluted tubules (PCT) in the kidney of anesthetized rats. Transtubular potassium concentration ([K+]) gradients were varied by altering the concentration of KCl in luminal perfusates, to which 32 mmol/l of the impermeant solute raffinose was also added to prevent net fluid reabsorption. The arithmetic mean transtubular [K+] gradient was highly predictive of net potassium flux, yielding an apparent K+ permeability of 31.9 ± 1.7 × 10−5 cm/s in the absence of fluid reabsorption. When compared using identical calculation techniques, we found this was not significantly different from the permeability derived in a previous study when fluid reabsorption was present [J. D. Kibble, M. Wareing, R. W. Wilson, and R. Green. Am. J. Physiol. 268 ( Renal Fluid Electrolyte Physiol. 27): F778–F783, 1995]. We conclude that fluid reabsorption does not affect the apparent permeability of the proximal tubule to potassium. The apparent permeability to86Rb, measured following its addition to luminal perfusates, was not significantly different from the value obtained for K+, suggesting that rubidium is a useful marker for net potassium movements in the PCT of the rat.
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Choi, Michael J., and Fuad N. Ziyadeh. "The Utility of the Transtubular Potassium Gradient in the Evaluation of Hyperkalemia." Journal of the American Society of Nephrology 19, no. 3 (2008): 424–26. http://dx.doi.org/10.1681/asn.2007091017.
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Vögelin, Marius, Richard Cathomas, Niklaus Kamber, and Thomas Fehr. "Hypokalaemic metabolic alkalosis, hypertension and diabetes: what is the link." BMJ Case Reports 12, no. 1 (2019): bcr—2018–227068. http://dx.doi.org/10.1136/bcr-2018-227068.
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Two years after diagnosis of a metastatic neuroendocrine gastrin-secreting tumour and after several cycles of chemotherapy and peptide receptor radionuclide therapy, a 56-year-old woman presented with hypokalaemic metabolic alkalosis, hypertension, leg oedema and new-onset diabetes mellitus. Further investigations revealed renal potassium loss confirmed by a transtubular potassium gradient of 16, fully suppressed serum aldosterone, but instead highly elevated blood levels of morning cortisol and adrenocorticotropic hormone as well as increased urinary excretion of glucocorticoid and mineralocorticoid metabolites. Ruling out other causes, paraneoplastic hypercortisolism was diagnosed. Pharmacological inhibition of the steroid 11β-hydroxylase with metyrapone resulted in complete resolution of metabolic alkalosis, hypokalaemia, hypertension, hyperglycaemia and leg oedema within 1 week.
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Chacko, M., JS Fordtran, and M. Emmett. "Effect of mineralocorticoid activity on transtubular potassium gradient, urinary [K]/[Na] ratio, and fractional excretion of potassium." American Journal of Kidney Diseases 32, no. 1 (1998): 47–51. http://dx.doi.org/10.1053/ajkd.1998.v32.pm9669423.
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Musso, Carlos, Vassilis Liakopoulos, Raul De Miguel, Nora Imperiali, and Luis Algranati. "Transtubular potassium concentration gradient: comparison between healthy old people and chronic renal failure patients." International Urology and Nephrology 38, no. 2 (2006): 387–90. http://dx.doi.org/10.1007/s11255-006-0059-5.
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Kaufman, J. S., and R. J. Hamburger. "Passive potassium transport in the proximal convoluted tubule." American Journal of Physiology-Renal Physiology 248, no. 2 (1985): F228—F232. http://dx.doi.org/10.1152/ajprenal.1985.248.2.f228.
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Potassium transport in the isolated proximal convoluted tubule (PCT) of the rabbit was studied to determine the importance of concentration-dependent passive processes in potassium reabsorption. Net potassium flux was measured with an initial perfusate potassium concentration of 4 mM and bath potassium concentration of 2, 4, or 6 mM. When bath concentration was 6 mM, there was net potassium secretion in both superficial (SF) and juxtamedullary (JM) PCT. When bath concentration was 2 mM, there was net reabsorption in both groups of tubules. The apparent permeability coefficients were found to be significantly higher in JMPCT (2.96 +/- 0.37 pmol X mm-1 X min-1 X mM-1) than in SFPCT (1.94 +/- 0.34 pmol X mm-1 X min-1 X mM-1). We also attempted to uncover an active potassium reabsorption process by inhibiting water flux, but not other transport processes, by the imposition of a transtubular osmotic gradient. When the perfusate was made 30 mosmol/kg H2O hypertonic to the bath, there was net fluid entry of 0.38 +/- 0.09 nl/min, accompanied by a significant decline in net potassium flux. The collected fluid-to-perfusate potassium concentration ratio was not significantly less than zero, thereby not providing evidence for active potassium reabsorption. These studies suggest that a primary mode of potassium reabsorption in this segment is due to its movement along a transepithelial gradient established by fluid reabsorption. We have been unable to identify an active component of potassium reabsorption.
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Lim, Young-Suk, Jin Suk Han, Kyung-Ah Kim, Jung-Hwan Yoon, Chung Yong Kim, and Hyo-Suk Lee. "Monitoring of transtubular potassium gradient in the diuretic management of patients with cirrhosis and ascites." Liver 22, no. 5 (2002): 426–32. http://dx.doi.org/10.1034/j.1600-0676.2001.01693.x.
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Sakaguchi, Taiki, Akio Hirata, Kazunori Kashiwase, et al. "Transtubular Potassium Concentration Gradient as a Surrogate Measure of Arterial Underfilling in Acute Decompensated Heart Failure." Circulation Journal 80, no. 9 (2016): 1965–70. http://dx.doi.org/10.1253/circj.cj-16-0437.
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Rodr�guez-Soriano, Juan, Mercedes Ubetagoyena, and Alfredo Vallo. "Transtubular potassium concentration gradient: a useful test to estimate renal aldosterone bio-activity in infants and children." Pediatric Nephrology 4, no. 2 (1990): 105–10. http://dx.doi.org/10.1007/bf00858819.
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Mabillard, Holly, and John A. Sayer. "SARS-CoV-2 and hypokalaemia: evidence and implications." F1000Research 9 (June 10, 2020): 587. http://dx.doi.org/10.12688/f1000research.24441.1.
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The global pandemic secondary to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is leading to unprecedented global morbidity and mortality. With a bewildering array of complications, renal involvement in various forms is common, including serum electrolyte derangements. Hypokalaemia secondary to SARS-CoV-2 was common in a reported Chinese cohort. Here we review the emerging evidence on hypokalaemia and SARS-CoV-2 infection, the potential pathophysiological mechanisms based on early clinical and histopathological data and important clinical implications. Mechanisms of hypokalaemia are multifactorial and so the electrolyte disturbance can be difficult to avoid. We provide further support to the theory of renin-angiotensin-aldosterone (RAS) activation, discuss the strengths and weaknesses of implicating RAS involvement and highlight the importance of calculating the transtubular potassium gradient to identify those at risk of hypokalaemia and its complications.
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Mabillard, Holly, and John A. Sayer. "Electrolyte Disturbances in SARS-CoV-2 Infection." F1000Research 9 (July 22, 2020): 587. http://dx.doi.org/10.12688/f1000research.24441.2.
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The global pandemic secondary to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is leading to unprecedented global morbidity and mortality. With a bewildering array of complications, renal involvement in various forms is common, including serum electrolyte derangements. Hypokalaemia secondary to SARS-CoV-2 was common in a reported Chinese cohort. Here we review the emerging evidence on hypokalaemia and SARS-CoV-2 infection, the potential pathophysiological mechanisms based on early clinical and histopathological data and important clinical implications. Mechanisms of hypokalaemia are multifactorial and so the electrolyte disturbance can be difficult to avoid. We provide further support to the theory of renin-angiotensin-aldosterone (RAS) activation, discuss the strengths and weaknesses of implicating RAS involvement and highlight the importance of calculating the transtubular potassium gradient to identify those at risk of hypokalaemia and its complications.
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Steele, A., H. deVeber, S. E. Quaggin, A. Scheich, J. Ethier, and M. L. Halperin. "What is responsible for the diurnal variation in potassium excretion?" American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 2 (1994): R554—R560. http://dx.doi.org/10.1152/ajpregu.1994.267.2.r554.
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Potassium excretion exhibits a diurnal pattern, with most excretion occurring close to noon in humans. Each component of the K+ excretion rate [urinary K+ concentration ([K+]) and flow rate] was measured and back-calculated to reflect events in the cortical collecting duct (CCD). Our purpose was to determine to what extent each component contributed to this diurnal variation in each 2-h portion of the day. In humans, K+ excretion rose threefold from nadir (0600 h) to peak (1200-1400 h), 18 h after the principal intake of K+. The variation in K+ excretion was due almost exclusively to changes in [K+] in the terminal CCD ([K+]CCD) rather than via changes in flow rate. In rats, the bulk of K+ excretion occurred shortly after eating. Both components of K+ excretion rose after meals; the rise in the [K+]CCD (3.3-fold) predominated at earlier times, and the rise in flow rate occurred later and was primarily a result of a higher rate of excretion of urea. The rise in [K+]CCD did not correlate with aldosterone levels or administration. A very large rise in the [K+]CCD only occurred in the presence of bicarbonaturia; the transtubular potassium concentration gradient was now close to 15 in the morning and evening.
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Lin, Shih-Hua, Surinder Cheema-Dhadli, Manjula Gowrishankar, Errol B. Marliss, Kamel S. Kamel, and Mitchell L. Halperin. "Control of excretion of potassium: lessons from studies during prolonged total fasting in human subjects." American Journal of Physiology-Renal Physiology 273, no. 5 (1997): F796—F800. http://dx.doi.org/10.1152/ajprenal.1997.273.5.f796.
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A deficit of K+ of close to 300 mmol develops in the first 2 wk of fasting, but little further excretion of K+ occurs, despite high levels of aldosterone and the delivery of ketoacid anions that are not reabsorbed in the distal nephron. Our purpose was to evaluate how aldosterone could have primarily NaCl-retaining, rather than kaliuretic, properties in this setting. To evaluate the role of distal delivery of Na+, four fasted subjects recieved an acute infusion of NaCl to induce a natriuresis. To assess the role of distal delivery of [Formula: see text], five fasted subjects were given an infusion containing NaHCO3. The natriuresis induced by an infusion of NaCl caused only a small rise in the rate of excretion of K+ (0.8 ± 0.1 to 1.9 ± 0.3 mmol/h); in contrast, when [Formula: see text]replaced Cl− in the infusate, K+ excretion rose to 8.3 ± 2.2 mmol/h, despite little excretion of[Formula: see text] (urine, pH 5.8) and similar rates of excretion of Na+. The transtubular K+ concentration gradient was 19 ± 3 with [Formula: see text] and 6 ± 2 with NaCl. We conclude that the infusion of NaHCO3 led to an increase in K+ excretion, likely reflecting an increased rate of distal K+secretion. With a low distal delivery of[Formula: see text], aldosterone acts as a NaCl-retaining, rather than a kaliuretic, hormone.
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Malik, Sundeep, Emily Lambert, Junhui Zhang, et al. "Potassium conservation is impaired in mice with reduced renal expression of Kir4.1." American Journal of Physiology-Renal Physiology 315, no. 5 (2018): F1271—F1282. http://dx.doi.org/10.1152/ajprenal.00022.2018.
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To better understand the role of the inward-rectifying K channel Kir4.1 (KCNJ10) in the distal nephron, we initially studied a global Kir4.1 knockout mouse (gKO), which demonstrated the hypokalemia and hypomagnesemia seen in SeSAME/EAST syndrome and was associated with reduced Na/Cl cotransporter (NCC) expression. Lethality by ~3 wk, however, limits the usefulness of this model, so we developed a kidney-specific Kir4.1 “knockdown” mouse (ksKD) using a cadherin 16 promoter and Cre-loxP methodology. These mice appeared normal and survived to adulthood. Kir4.1 protein expression was decreased ~50% vs. wild-type (WT) mice by immunoblotting, and immunofluorescence showed moderately reduced Kir4.1 staining in distal convoluted tubule that was minimal or absent in connecting tubule and cortical collecting duct. Under control conditions, the ksKD mice showed metabolic alkalosis and relative hypercalcemia but were normokalemic and mildly hypermagnesemic despite decreased NCC expression. In addition, the mice had a severe urinary concentrating defect associated with hypernatremia, enlarged kidneys with tubulocystic dilations, and reduced aquaporin-3 expression. On a K/Mg-free diet for 1 wk, however, ksKD mice showed marked hypokalemia (serum K: 1.5 ± 0.1 vs. 3.0 ± 0.1 mEq/l for WT), which was associated with renal K wasting (transtubular K gradient: 11.4 ± 0.8 vs. 1.6 ± 0.4 in WT). Phosphorylated-NCC expression increased in WT but not ksKD mice on the K/Mg-free diet, suggesting that loss of NCC adaptation underlies the hypokalemia. In conclusion, even modest reduction in Kir4.1 expression results in impaired K conservation, which appears to be mediated by reduced expression of activated NCC.
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Beck, Nam-Seon, Yeon-Oh Jeong, Kyung-Hee Lee, Eun-Mi Jun, Joung-Il Im, and Sae-Yong Hong. "Chronic Liver Disease Primarily Presenting with Motor Weakness by Intractable Hypokalemia with Combined Respiratory Alkalosis and Chronic Diarrhea: A Case Report." Case Reports in Gastroenterology 19, no. 1 (2025): 165–72. https://doi.org/10.1159/000544099.
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Introduction: Most patients with compensated cirrhosis remain asymptomatic. However, with the onset of decompensation, electrolyte and acid-base disturbances are frequent in patients with chronic liver disease, including hypokalemia. We encountered a case of chronic liver disease with portal hypertension, primarily presenting with motor weakness caused by intractable hypokalemia, hypoxia-associated respiratory alkalosis, and chronic diarrhea. Case Presentation: A 54-year-old male presented to the emergency department with motor weakness. He reported experiencing exertional dyspnea and watery diarrhea for the past 3 months, approximately ten times daily. Arterial blood gas analysis indicated hypoxia and hypocapnia compatible with chronic respiratory alkalosis. The transtubular potassium gradient was 1.69, and the aldosterone/renin ratio was 17.6 (ng/dL)/(ng/mL/h). The patient had a 30-year history of consuming 360–720 mL of 20% alcohol almost daily. Abdominal computed tomography revealed multiple regenerative and dysplastic nodules in the liver, splenomegaly, ascites, esophageal varices, and diffuse edematous wall thickening in the bowel, suggesting portal hypertensive enteropathy. Computed tomography of the lungs showed no specific abnormalities in the lungs, pleura, or thoracic wall. Conclusion: We present a case of liver cirrhosis complicated by intractable hypokalemia, respiratory alkalosis, portal hypertension, and chronic diarrhea. A 24-h urine analysis showed renal excretion levels of Na+, K+, and Cl− at 6.0, 2.5, and 11.0 mmol, respectively, suggesting renal retention of these electrolytes. Meanwhile, the serum levels of Na+, K+, and Cl− were 136, 1.8, and 98 mEq/L, respectively, indicating a preserved balance of sodium and chloride but not potassium. This case underscores the importance of clinicians considering both liver cirrhosis-associated hypoxia and chronic liver disease-induced chronic diarrhea as potential underlying causes, especially when more common causes of hypokalemia have been excluded.
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Olenovych, О. А. "Pathogenetical aspects of tubulointerstitial syndrome development in alloxan-induced experimental diabetes mellitus." Reports of Vinnytsia National Medical University 25, no. 1 (2021): 17–21. http://dx.doi.org/10.31393/reports-vnmedical-2021-25(1)-03.
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Annotation. The aim of our study was to explore the pathogenetical aspects of tubulointerstitial syndrome development in alloxan-induced experimental diabetes mellitus. The experiments were carried out on 20 white non-linear mature male rats, 10 with experimental diabetes mellitus (EDМ) induced by intraperitoneal administration of alloxan at a dose of 160 mg/kg of body weight, 10 intact rats served as the control group. 25 days after administration of the diabetogenic substance, the animals were withdrawn from the experiment. The concentration of sodium and potassium ions in urine and blood plasma samples was determined, followed by calculation (considering water-induced 2-hour diuresis and endogenous creatinine clearance) of glomerular filtration rate, electrolyte excretion, their filtration rate, absolute and relative reabsorption, clearance, their proximal and distal renal transport. Removed after decapitation rats’ kidneys were dissected to 3 parts – renal cortex, medulla and papilla, sodium and potassium content was determined in water-extract of the corresponding part of the renal parenchyma, and papillary-cortical, papillary-medullar and medullary-cortical concentration ion gradients were calculated. Significant suppression of papillary-medullar and papillary-cortical concentration sodium gradients, as well as a slight limitation of its medullary-cortical gradient were established. The concentration potassium gradients were significantly reduced. Statistical processing of the obtained data was carried out with the determination of the average value, standard deviations. To assess the probability of the difference between the study groups used non-parametric Mann-Whitney ranking criterion according to the algorithms implemented in the computer program “Statistica for Windows”, “Version 8.0”. There was a decrease of the sodium-potassium ratio in urine, enhanced urinary excretion of potassium and an increase of its content in urine, as well as intensification of absolute transtubular sodium transport due to equivalent augmentation of the filtration charge of this cation, increase of proximal sodium reabsorption and, to a lesser degree, – of distal one. The distal and proximal sodium reabsorption, reduced to a unit of active nephrons, was found to be decreased, and the relative reabsorption of the cation significantly exceeded the control values, contributing to the limitation of natriuresis. The results of the study suggest that in 26-day alloxan-induced experimental diabetes hemodynamic-hyperperfusion overload on the tubular apparatus of the kidney causes the development of relative insufficiency of the proximal and distal tubules, disorders of hormone-dependent reabsorption of cations, limitation of regulatory influence of aldosterone and ADH with further tubulointerstitial disturbances that unable adequate osmotic concentration of urine.
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Tamaki, S., T. Yamada, T. Watanabe, et al. "Effect of empagliflozin as add-on therapy on transtubular potassium concentration gradient in patients with type 2 diabetes hospitalized for acute decompensated heart failure." European Heart Journal 41, Supplement_2 (2020). http://dx.doi.org/10.1093/ehjci/ehaa946.1228.
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Abstract Background The transtubular potassium concentration gradient (TTKG) has been reported to be a marker of renal aldosterone bioactivity, and has been shown to be a surrogate of arterial underfilling in patients with acute decompensated heart failure (ADHF). Moreover, high TTKG at discharge has been shown to be associated with poor prognosis in ADHF patients. Empagliflozin, one of the sodium glucose cotransporter 2 inhibitors, has been shown to reduce the risk of cardiovascular mortality in patients with type 2 diabetes mellitus (T2D) and cardiovascular disease. However, little is known about the effect of empagliflozin as add-on therapy on TTKG in T2D patients with ADHF. Purpose We sought to elucidate the effect of empagliflozin as add-on therapy on TTKG in T2D patients with ADHF. Methods We enrolled 58 consecutive T2D patients admitted for ADHF. On admission, enrolled patients were randomly assigned in a 1:1 ratio to either empagliflozin add-on therapy (EMPA(+)) or conventional glucose-lowering therapy (EMPA(−)). All patients in EMPA(+) group received empagliflozin (10 mg/day) throughout the study period. Left ventricular ejection fraction (LVEF) was measured at baseline using echocardiography. Body weight and vital signs, such as blood pressure and heart rate, were measured, and blood and urine samples were collected at baseline and 1, 2, 3 and 7 days after randomization. The TTKG was measured using the first morning urine samples collected on each day. TTKG was calculated according to the following equation: TTKG = (Ku/Ks)×(plasma osmolality/urine osmolality), where Ku is urine potassium concentration and Ks is serum potassium concentration, as previously reported. Results Thirty patients were assigned to the EMPA(+) group, and 28 patients were assigned to the EMPA(−) group. There were no significant baseline differences in LVEF, plasma B-type natriuretic peptide (BNP) level, body mass index, or serum creatinine level between the EMPA(+) and EMPA(−) groups. TTKG did not significantly differ between the two groups at baseline. However, seven days after randomization, plasma BNP level was significantly lower in the EMPA(+) group than in the EMPA(−) group (median 227 [IQR 114–381] pg/mL vs 362 [227–554] pg/mL, p=0.0294). Furthermore, TTKG of the EMPA(+) group was significantly lower at 2, 3 and 7 days after randomization (Figure). Conclusions This study demonstrated that empagliflozin as add-on therapy can lower TTKG in T2D patients with ADHF. Figure 1 Funding Acknowledgement Type of funding source: None
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Wouda, Rosa D., Martin Gritter, Micky Karsten, et al. "Kaliuresis and Intracellular Uptake of Potassium with Potassium Citrate and Potassium Chloride Supplements: A Randomized Controlled Trial." Clinical Journal of the American Society of Nephrology, June 29, 2023. http://dx.doi.org/10.2215/cjn.0000000000000228.
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Background: A potassium replete diet is associated with lower cardiovascular risk, but may increase the risk of hyperkalemia, particularly in people using renin–angiotensin–aldosterone system inhibitors (RAASi). We investigated whether intracellular uptake and potassium excretion after an acute oral potassium load depend on the accompanying anion and/or aldosterone and whether this results in altered plasma potassium change. Methods: In this placebo-controlled interventional cross-over trial including 18 healthy individuals, we studied the acute effects of one oral load of potassium citrate (40 mmol), potassium chloride (40 mmol), and placebo in random order after overnight fasting. Supplements were administered after a 6-week period with and without lisinopril pretreatment. Linear mixed effect models were used to compare blood and urine values before and after supplementation, and between the interventions. Univariable linear regression was used to determine the association between baseline variables and change in blood and urine values after supplementation. Results: During 4-hour follow-up, the rise in plasma potassium was similar for all interventions. After potassium citrate, both red blood cell (RBC) potassium—as measure of the intracellular potassium—and transtubular potassium gradient (TTKG)—reflecting potassium secretory capacity—were higher than after potassium chloride or potassium citrate with lisinopril pretreatment. Baseline aldosterone was significantly associated with TTKG after potassium citrate, but not after potassium chloride or potassium citrate with lisinopril pretreatment. The observed TTKG change after potassium citrate was significantly associated with urine pH change during this intervention (R=0.60, P<0.001). Conclusions: With similar plasma potassium increase, RBC potassium uptake and kaliuresis were higher after an acute load of potassium citrate as compared to potassium chloride alone or pretreatment with lisinopril.
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Ruiz Sanchez, Jorge Gabriel, Alfonso Luis Calle-Pascual, Miguel Angel Rubio-Herrera, Maria Paz De Miguel Novoa, Emilia Gomez-Hoyos, and Isabelle Runkle. "Isolated hypoaldosteronism is a cause of hypovolemic, but not euvolemic, hyponatremia." Endocrine Connections, January 2024. http://dx.doi.org/10.1530/ec-23-0430.
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INTRODUCTION. Hypoaldosteronism is characterized by hyperkalemia, and/or hypovolemic hyponatremia (HH), often accompanied by metabolic acidosis. HH is typical of hypoaldosteronism, whereas euvolemic hyponatremia (EH) is not. The purpose of the current study is to describe the characteristics of hyponatremia in hypoaldosteronism, and elucidate whether EH can be considered part the disease’s spectrum. METHODS. In a hypoaldosteronism cohort, we analyzed the factors associated with hyponatremia, comparing the characteristics of EH and HH and their associated factors. Correlation analyses of mineralocorticoid biomarkers, such as the transtubular potassium gradient (TTKG), and the urinary Na+/K+ ratio (UNa+/UK+) with serum and urinary electrolytes were performed in both types of hyponatremia. RESULTS. Of 112 hypoaldosteronism episodes, 77.7% were ≥ 65 years old, 44.6% were women and 80 (71.4%) had hyponatremia. Hyponatremia was negatively associated with the presence of chronic kidney disease, and positively with a hypovolemic state, malnutrition, a prior history of hyponatremia and glucocorticoid therapy. HH: 61/80 and EH: 19/80 episodes. HH was associated with an age ≥ 65 years and the use of diuretics, as well as factors related to an aldosterone deficit and/or mineralocorticoid resistance. In HH, but not in EH, urinary potassium was correlated with the TTKG, and urinary sodium with both the TTKG and the UNa+/UK+. CONCLUSION: Both HH and EH can be observed in hypoaldosteronism. However, only the former would be related to insufficient mineralocorticoid activity.
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Halperin, Mitchell L. "Assessing the renal response in patients with potassium disorders: a shift in emphasis from the TTKG to the urine K+/creatinine ratio." African Journal of Nephrology 20, no. 1 (2017). http://dx.doi.org/10.21804/20-1-2453.
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This article briefly reviews the reasons for replacing the transtubular K+ gradient (TTKG) with the urine K+/creatinine ratio, as a tool for evaluating the response of the kidney in patients with potassium disorders. An appreciation of the magnitude and importance of the intrarenal recycling of urea led to the realization that a large amount of urea is reabsorbed daily in the terminal collecting duct and that this renders invalid the assumption, used by the TTKG, that there is minimal solute reabsorption downstream of the cortical collecting duct (CCD). The urine-to-plasma osmolality ratio can therefore not be used to calculate the volume of fluid exiting the CCD nor the concentration of K+ in the luminal fluid in this nephron segment. We now recommend the use of the K+/creatinine ratio in random urine samples to estimate the rate of K+ excretion. A ratio of less than 1.5 mmol K+/mmol creatinine would be expected if the kidney is responding appropriately to hypokalaemia from a non-renal cause, and a ratio greater than 20 mmol K+/mmol creatinine would be appropriate as the renal response to hyperkalaemia.
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Davids, M. Razeen. "Editorial note." African Journal of Nephrology 20, no. 1 (2017). http://dx.doi.org/10.21804/20-1-2452.
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Now that we have successfully migrated to our new online platform, AJN has taken the additional step of adopting a “publish-as-you-go” strategy. Articles will be published once they have been accepted and there will no longer be the usual wait until the next issue is published. New articles will be added throughout the year and will therefore be available to be read and cited much sooner. The latest articles which we are now publishing include a short review by Halperin on the assessment of the renal response in patients with potassium disorders. Halperin first gave us the well-known transtubular K+ gradient (TTKG) but in recent years has been recommending the use of the urine K+/creatinine ratio instead. In this article he explains the reasons for this change. Kapembwa et al. present their data on technique survival in patients on peritoneal dialysis (PD) at Tygerberg Hospital in Cape Town. Successfully maintaining patients on PD is especially important when a PD-first policy is being followed, as is the case at their centre. The issue of the access of rural patients with chronic kidney disease to healthcare is the topic of the paper by Singh et al., who report on referral patterns at a tertiary centre in Durban, South Africa. The paper by Camara et al., from the Free State province, South Africa, describes the outcomes of patients with acute kidney injury who needed continuous renal replacement therapy. In their cohort, patients with HIV infection were substantially younger and had a much worse outcome. Finally, the report by Makhoba et al. describes a case of osseous metaplasia in a renal allograft.
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González, David Menéndez, Consolación Rosado, Gilda Carreño Cornejo, et al. "#2026 Hypokalemia associated to neuroendocrine carcinoma of the cervix." Nephrology Dialysis Transplantation 39, Supplement_1 (2024). http://dx.doi.org/10.1093/ndt/gfae069.1799.
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Abstract Background and Aims Hypokalemia is one of the most common electrolyte disorders seen in clinical practice. Hypokalemia can be caused by decreased intake of potassium, redistribution of potassium (K+) in cells or by excessive gastrointestinal losses or renal losses. In this setting, hypokalemia may also be caused by the paraneoplastic production of ectopic adrenocorticotropic hormone (ACTH) by some tumors. Cancer of the uterine cervix is the fourth common cancer affecting women worldwide and the fourth most common gynecologic cancer in Spain. Neuroendocrine carcinoma of the cervix represents about 2% of all cervical neoplasms. Method We report the case of a 44-year-old Peruvian woman with hypokalemia who was diagnosed with Cushing syndrome secondary to paraneoplastic production of ACTH by neuroendocrine carcinoma of cervix. Results Patient was overweight and affected by uterine myoma and anemia without further investigations. She was admitted to our hospital due to lower back pain, leg swelling and constipation. Blood pressure was normal, chest radiography did not show abnormal findings and ECG showed the U wave. Laboratory tests at admission revealed hypokalemia (2.3 mmol/L), metabolic alkalosis, anemia (hemoglobin 9.5 g/dL), hyperkaliuria (K+ urine/Creatinine urine 70 mmol/g) with an elevated transtubular potassium gradient (TTKG=12) and normal renal function. Laboratory data are presented in Table 1. She developed hypertension in the first day of hospitalization. Renin, aldosterone and cortisol tests was performed. Hypercortisolism was observed and confirmed with 24-hour urinary cortisol excretion. Because of an elevated ACTH (263 pg/mL), pituitary magnetic resonance imaging was performed without lesions. Whole-body computed tomography revealed a cervical mass. PET scan showed pelvic, adrenal, hepatic and local lymphadenopathy activity (see Fig. 1). After the histopathological study, diagnostic of small cell neuroendocrine carcinoma of the cervix was made. Chemotherapy therapy was initiated with cisplatin/etoposide regimen. The patient decide to return to Peru because of the poor prognosis of her illness. At discharge, potassium level was 3 mmol/L despite the treatment with spironolactone, ramipril, losartan and oral potassium chloride (160 mmol). Conclusion Hypokalemia is a common clinical disorder. In some patients it may be caused by an increased mineralocorticoid activity due to ectopic ACTH-secreting tumors. Applying diagnostic algorithms to electrolyte disorders, beyond their simple treatment, can unmask secondary causes and serious diseases.
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Wang‐France, Jun, Bangchen Wang, Huaqing Li, and Steven Sansom. "Renal handling of potassium in the type 2 Bartter's mouse on a low Na, high K diet (LNaHK)." FASEB Journal 31, S1 (2017). http://dx.doi.org/10.1096/fasebj.31.1_supplement.857.13.
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Mice on a low Na, high K diet (LNaHK; 0.01% Na, 5% K, 5% carbonate/citrate/Cl) maintain K balance because of the dietary effect to stimulate high distal flow and elicit a very high plasma aldosterone (P[aldo]) that maximally increases the activity of the epithelial Na channel (ENaC). Presumably, the high distal flow stimulates K secretion by the large, Ca‐activated K channel (BK) while the enhanced ENaC‐mediated Na reabsorption increases the driving force for K secretion via both BK and the renal outer medullary K channel (ROMK). However, the notion that ROMK plays a role in K secretion in the distal nephron of mice on LNaHK has not been examined in ROMK knockout mice (KO). To this end, we determined plasma aldosterone levels (P[aldo]; ELISA) and studied the renal handling of K in WT and KO (129/SvJ) mice on LNaHK (4–7 days) with metabolic cage experiments. Glomerular filtration rate (GFR) was measured with FITC‐inulin in conscious mice. On a control diet, there was no difference between WT and KO in the rate of K excretion (UKV; 516.1±63.4 and 521.3±64.1 mmol/day). On LNaHK, the UKV in KO was slightly but significantly lower than WT (1867±312.8 and 2483±92.1 mmol/day). Compared with WT on a control diet (0.3% Na, 0.6% K), KO exhibited a 4‐fold greater urine volume (KO = 5.4±0.6 and WT = 1.4±0.2 ml/day), a reduction in urine osmolality (658±63 and 3253±402 mOsm) but no change in plasma K (P[K]; 4.7±0.8 and 4.5±0.2 mM). Compared to WT on LNaHK, KO exhibited a higher urine volume (6.2±0.6 and 4.3±0.4 ml/day), a reduction in urine osmolality (660±43 and 1708±139 mOsm) but a reduced GFR (177.6±34.1 and 452.9±28.1 ml/day). The reduced GFR of KO was probably the result of a failure to retain Na and volume with a 2‐fold urinary Na loss (UNaV) compared with WT (64.9±11 and 30.8±4.1 mmol/day) and a three‐fold greater P[aldo] (9558±75 and 3717±470 pg/ml). However, KO on LNaHK still maintained K balance with a slightly, but not significantly, elevated P[K] (5.6±0.7 and 4.9±0.2 mM), a 2‐fold increased fractional excretion of K (193.8±52.1% and 97.7±8.0%) and a similar transtubular K gradients (TTKG; 27.4±2.8 and 26.3±1.4), compared with WT. These data indicate that reduced K excretion in KO on LNaHK is caused by reduced GFR due to inadequate Na and volume retention. ROMK of the aldosterone‐sensitive distal nephron does not contribute to K secretion of mice on LNaHK to maintain K balance.Support or Funding InformationThis project is supported by NIDDK grants 3451702067001 and 3451702071006.
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Sablón-González, Nery, Yanet Parodis-Lopez, Maria Belen Alonso-Ortiz, Angélica Laurin, Emmanuel Andres, and Noel Lorenzo Villalba. "Recurrent Episodes of Hypokalaemia during Treatment with Inhaled Beta-2 Agonist Revealing Gitelman Syndrome, an Uncommon Clinical Entity." European Journal of Case Reports in Internal Medicine, October 20, 2022. http://dx.doi.org/10.12890/2022_003605.
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A 28-year-old female patient was hospitalized for mild–moderate hypokalaemia which was persistent despite discontinuation of beta-2 agonist bronchodilator treatment. Her past medical history was relevant for two episodes of severe hypokalaemia after active inhaled beta-2 agonist treatment for asthma crisis. Investigations revealed increased potassium in spot urine with a transtubular potassium gradient <4. A 24-hour urine analysis showed hypophosphaturia, hypocalciuria, hypomagnesuria and normal urine prostaglandins in favour of Gitelman syndrome. Oral potassium supplementation was started and genetic studies were recommended.
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S, k. Sinha, and Manghani. R. "CONGENITAL ADRENAL HYPERPLASIA: PRESENTING WITHHYPOCORTISOLISM; SEVEREHYPOCALCAEMIA; HYPOKALAEMIA AND HYPOGONADOTROPIC HYPOGONADISM." March 16, 2018. https://doi.org/10.5281/zenodo.1237500.
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Congenital adrenal hyperplasia in milder forms is not very uncommonWe here report such a case of CAH who defaulted in taking glucocorticoid treatment after taking for nineteen years since the age of two years .For two years the patient did not take replacement steroid.He developed hypertension one year after discontinuation for which he was prescribed antihypertensive . The patient had been taking Indapamide for one year to control hypertension. His condition deteriorated for last two months and he lost weight, became anorectic ,started taking food sparingly. He presented to the hospital with severe weakness, pain ab-domen,nausea, vomiting,found to be hypokalaemic,hypocortisolaemic,hypocalcaemic and developed tetany 2-3 days after admission.
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Karapurkar, Sonia, Radha Ghildiyal, Nikita Shah, Rachna Keshwani, and Sujata Sharma. "Early detection of glomerular dysfunction and renal tubulopathy in children with sickle cell disease in India." Journal of Tropical Pediatrics 69, no. 2 (2023). http://dx.doi.org/10.1093/tropej/fmad019.
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Abstract Background Sickle cell disease causes microvascular occlusion in different vascular beds. In kidneys, it leads to occult glomerular dysfunction causing asymptomatic microalbuminuria, proximal tubulopathy causing hyposthenuria and increased free water loss and distal tubulopathy causing poor urine acidification. We studied the prevalence of various types of renal dysfunction, the ability of different tests to detect it at an early stage and the correlation of these parameters in children receiving hydroxyurea (HU). Procedure Fifty-six children (sample size calculated using SAS9.2 package) attending paediatric clinical services in a tertiary care hospital between 2 and 12 years of age diagnosed by high-performance liquid chromatography (HPLC) were enrolled. Their demographic and laboratory data including renal and urine parameters were collected. Parameters like fractional excretion of sodium (FeNa), trans tubular potassium gradient (TtKg) and free water clearance (TcH2O) were derived by calculations. Data were analysed using IBM SPSS Version 21.0 and Microsoft Office Excel 2007. Results We found a significant number of children to have microalbuminuria (17.8%), hyposthenuria (30.4%) and impaired renal tubular potassium excretion (TtKg) (81.3%). A significant correlation was found between the dose of HU with urine osmolality (p &lt; 0.0005) and free water clearance (p = 0.002), while all parameters showed a significant correlation with compliance with HU. Derangement in urine microalbumin and TcH2O correlated significantly with low mean haemoglobin levels (&lt;9 g/dl). Conclusion Renal dysfunction is common in children with SCD and can be detected early using simple urine parameters and can be prevented with an early and appropriate dosage of HU with good compliance.
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Lee, Seon Yeong, Jung Tak Park, Young Su Joo, et al. "Association between the transtubular potassium gradient and progression of chronic kidney disease: results from KNOW-CKD." Journal of Nephrology, March 23, 2021. http://dx.doi.org/10.1007/s40620-021-01019-9.
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Petini, M., M. Drigo, M. Caldin, and A. Zoia. "Diagnostic predictivity of transtubular potassium gradient for primary hypoadrenocorticism in hyperkalemic dogs: a cross‐sectional study." Journal of Small Animal Practice, April 10, 2023. http://dx.doi.org/10.1111/jsap.13613.
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Manolasya, Venkat, Kiran Peerappa, Praveena Prasanth, Bayyareddy Venkatarami Reddy, and Vishnubhotla Sivakumar. "Gitelman’s syndrome presenting as acute flaccid quadriparesis." Journal of Clinical and Scientific Research, June 11, 2025. https://doi.org/10.4103/jcsr.jcsr_37_24.
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Abstract A 64-year-old male patient presented with a history of generalised weakness and fatigue for the past 3 days. Past history of similar complaints during the past 3 years had resulted in recurrent hospitalisation elsewhere; hypokalaemia was documented but no further diagnostic work-up had been done. At admission, the general physical examination was unremarkable. Neurological examination revealed hyporeflexic flaccid quadriparesis. Other systems examination was normal. Laboratory testing revealed hypokalaemia (serum potassium 1.7 mEq/L) and arterial blood gas analysis revealed metabolic alkalosis. Diagnostic work-up revealed renal loss of potassium (urinary potassium: 84.4 mEq/g) creatinine secondary to increased distal potassium secretion (transtubular potassium gradient >4). Serum magnesium (2.1 mg/dL) and serum calcium (8.5 mg/dL) were normal. Antinuclear antibody profile tested negative. Urinary chloride and urinary calcium levels were 99.9 mEq/L, 1.69 mg/dL, respectively. Urine calcium–creatinine ratio was 0.02. A diagnosis of Gitelman’s syndrome (GS) was made. The patient was treated with potassium-sparing diuretics, potassium and magnesium supplementation and responded well to treatment. At 1 month after discharge, serum potassium was 3.4 mEq/L and the patient was doing well on follow-up. The present case highlights the importance of considering GS in the differential diagnosis in patients presenting with recurrent episodes of hypomagnesemia with hypokalaemia, hyporeflexic flaccid quadriparesis.
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Sakaguchi, T., A. Hirata, K. Kashiwase, Y. Higuchi, and Y. Yasumura. "144The transtubular potassium concentration gradient as a predictive index of clinical tissue hypoperfusion in patients with acute decompensated heart failure." European Heart Journal 38, suppl_1 (2017). http://dx.doi.org/10.1093/eurheartj/ehx501.144.
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Ambarsari, Cahyani Gita, Habibah Azzahra Putri Agianda, Meilania Saraswati, and Jon Jin Kim. "Dent Disease 1 Presented Early with Bartter-Like Syndrome Features and Rickets: a Case Report." Case Reports in Nephrology and Dialysis, January 21, 2025, 1–24. https://doi.org/10.1159/000543719.
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Introduction: Dent disease (DD) is characterized by a triad of low-molecular-weight proteinuria, hypercalciuria, and nephrocalcinosis/nephrolithiasis. However, some cases were confounded by other clinical symptoms and signs, namely hypokalemia and rickets, which resulted in misleading diagnoses. A diagnosis of DD could be delayed even in high-resource countries due to its variability of phenotypes and rarity, causing a lack of awareness in both medical practitioners and parents. Moreover, in low-resource countries, laboratory test limitations can hinder the diagnosis. Case presentation: A thirteen-year-old boy presented with an acute episode of severe hypokalemia following vomiting due to COVID medication side effects. He had lower extremities weakness, salt craving, and polydipsia since childhood which were not thought to be unusual by the parents. He had a history of intrauterine polyhydramnios and maternal miscarriages. A physical examination showed hypotension, short stature, and genu valgum. His laboratory workup displayed hypokalemic metabolic alkalosis and increased urine potassium, chloride, transtubular potassium gradient, and calcium/creatinine ratio. He also had hypophosphatemia, hypomagnesemia, and decreased kidney function. Severe osteopenia was prominent on radiologic examination of all extremities. Subsequent laboratory samples sent overseas revealed low-molecular-weight proteinuria and a pathogenic variant in the CLCN5 gene confirming X-linked Dent disease 1. Conclusion: This case report highlights the importance of considering DD in differential diagnoses of children with the pseudo-Bartter syndrome, that is, renal salt and potassium wasting, with or without hypercalciuria and nephrocalcinosis. Additionally, in children with rickets and proteinuria, urinary low-molecular-weight protein measurement could assist in screening for the possibility of DD, particularly in low-resource settings.
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Torrente, Carlos, Patricia Bou, Marta Riba, Dania Fernández, and Luis Bosch. "Refractory Hyperkalemia With Type 4 Renal Tubular Acidosis Associated With Tubulointerstitial Nephritis and Renal Papillary Necrosis Following Intravenous Lipid Emulsion Therapy in a Cat." Journal of Veterinary Emergency and Critical Care, April 20, 2025. https://doi.org/10.1111/vec.13462.
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ABSTRACTObjectiveTo describe type 4 renal tubular acidosis (RTA) and acquired pseudohypoaldosteronism in a cat with acute kidney injury (AKI) presumably associated with lipid infusion therapy for permethrin toxicosis.Case SummaryA 1‐year‐old neutered male cat presented with acute weakness, ataxia, fasciculations, tremors, hyperthermia, and seizures resulting from permethrin toxicosis. Upon admission, IV diazepam and 20% IV lipid emulsion were administered. Forty‐eight hours after discharge, the patient was readmitted for lethargy, anorexia, polyuria, and vomiting. Upon admission, the patient exhibited signs of depression, dehydration, and moderate hypoperfusion. Initial assessments included CBC, serum biochemistry profile, and urinalysis. Further diagnostic workup and abdominal point‐of‐care ultrasound revealed clinical findings compatible with AKI. Laboratory analysis confirmed severe hyperkalemia, hyperchloremic normal anion gap metabolic acidosis, decreased fractional excretion of potassium, and decreased transtubular potassium gradient in the urine, all consistent with a diagnosis of secondary or acquired pseudohypoaldosteronism and type 4 RTA. Emergency medical treatment for hyperkalemia was initiated, but control of serum potassium concentration was unsuccessful. Peritoneal dialysis (PD) and general supportive care were initiated 24 h after admission. Mineralocorticoid support (continuous rate infusion of hydrocortisone) was initiated 4 days after admission due to suspected deficiency/resistance to aldosterone at the distal nephron. Unfortunately, despite PD, refractory hyperkalemia persisted, and the cat died 16 days after admission. Histopathological examination confirmed an acute and severe renal papillary necrosis.New or Unique InformationTo the authors’ knowledge, this is the first description of type 4 RTA in a cat. Furthermore, we hypothesize that, according to the histopathological findings, this presentation of AKI may be secondary to the use of IV lipid emulsion for permethrin toxicosis, a complication not previously reported in the veterinary literature.
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Suetani, Y., Y. Iida, K. Hirose, et al. "Urine osmolality predicts worsening renal function and poor prognosis in acute decompensated heart failure." European Heart Journal 43, Supplement_2 (2022). http://dx.doi.org/10.1093/eurheartj/ehac544.1088.
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Abstract Background/Purpose Worsening renal function (WRF) can sometimes occur in the patients with acute decompensated heart failure (ADHF) and increase the risk of morbidity and mortality (1). In a previous study, it was reported that fractional excretion of sodium (FENa) reflects net sodium reabsorption from nephron segments and predicts WRF during treating ADHF (2). On the other hand, recently the new drugs which approach urine concentration mechanism and affect urine osmolality (U-OSM), such as tolvaptan and sodium-glucose cotransporter-2 inhibitor, have begun to be widely used as treatment of heart failure. Thus, we focused on U-OSM, which reflects not only sodium handling but also water excretion controlled by the collecting duct, and evaluated the association between WRF and U-OSM. Moreover, previous studies have demonstrated that FENa, fractional excretion of urea nitrogen and transtubular potassium concentration gradient are markers for long-term prognosis in patients with ADHF (3–5). Therefore, we also studied whether U-OSM can predict prognosis in ADHF. Methods A total of 157 patients admitted to our hospital because of a primary diagnosis of ADHF from February 2020 through July 2021 were retrospectively reviewed. U-OSM in the spot urinary samples were examined within 72 hours after admission. U-OSM was calculated based on the following validated formula (6): U-OSM = 1.07 × {2 × [urine sodium (mEq/L)] + [urine urea nitrogen (mg/dL)]/2.8 + [urine creatinine (mg/dl)] × 2/3} + 16.2. The primary outcome was the occurrence of WRF during hospitalization. WRF was defined as increased serum creatinine ≥0.3 mg/dL from baseline (7). The secondary outcome was the occurrence of ADHF readmission and all-cause death within 180 days after discharge. Results Primary Outcome. WRF developed in 46% of all patients. In the patients that developed WRF during hospitalization, U-OSM was significantly lower than in the patients without WRF (366±106 mOsm/L versus 430±128 mOsm/L; P&lt;0.001). Receiver operating characteristic curve analysis revealed the optimal cutoff values of U-OSM was 403 mOsm/L (AUC 0.64; 95% CI: 0.56–0.72; P&lt;0.001) to predict the WRF (Figure 1). On multivariable logistic regression analysis, U-OSM (OR, 1.99, 95% CI: 1.27–3.12; p=0.003) and serum creatinine (OR, 1.00, 95% CI: 0.99–1.00; P=0.009) were independent predictors of WRF. Secondary Outcome. There were 34 patients (22%) readmitted and 9 patients (6%) died within 180 days after discharge. ROC curve analysis revealed the optimal cutoff values of U-OSM as 349 mOsm/L (C-statistic 0.74; 95% CI: 0.65–0.83; P&lt;0.001) to predict ADHF readmission and all-cause death within 180 days (Figure 2A). On Kaplan-Meier analysis, the secondary outcome was significantly higher in patients with U-OSM&lt;349 mOsm/L (u-OSM≥349, 57%, U-OSM&lt;349, 43%; HR, 0.99; 95% CI: 0.99–1.00, P&lt;0.001) (Figure 2B). Conclusion U-OSM on admission may be a predictor of WRF and a prognostic marker in ADHF patients. Funding Acknowledgement Type of funding sources: None.