Books on the topic 'Glomerulonephritis, pathology'

This chapter discusses renal pathology, including acute kidney injury (AKI), chronic kidney disease (CKD), nephrotic syndrome, hereditary renal diseases, Alport’s syndrome and thin basement membrane lesion, hypertensive nephropathy, diabetic nephropathy, minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), membranous glomerulopathy, glomerulonephritis, IgA nephropathy, post-infectious glomerulonephritis, C3 glomerulopathy, anti-glomerular basement membrane disease, monoclonal gammopathy-associated kidney disease, acute tubular injury, acute tubulointerstitial nephritis, reflux nephropathy, and obstructive nephropathy.

Immunoglobulin A (IgA) nephropathy is the most common primary glomerulonephritis. It runs a slow and sometimes relentless clinical course with consequent end-stage renal failure in 35–40% of patients 25–30 years after first clinical presentation. The pathology is characterized by deposition of macromolecular (polymeric) IgA1 in the glomerular mesangium, proliferation of mesangial cells, increased synthesis of extracellular matrix, and infiltration of macrophage, monocytes, and T cells.

The urinary system is the primary target of Schistosoma haematobium infection, which leads to granuloma formation in the lower urinary tract that heals with fibrosis and calcification. While the early lesions may be associated with distressing acute or subacute symptoms, it is the late lesions that constitute the main clinical impact of schistosomiasis. The latter include chronic cystitis, ureteric fibrosis, ureterovesical obstruction or reflux which may lead to chronic pyelonephritis. Secondary bacterial infection and bladder cancer are the main secondary sequelae of urinary schistosomiasis.The kidneys are also a secondary target of S. mansoni infection, attributed to the systemic immune response to the parasite. Specific immune complexes are responsible for early, often asymptomatic, possibly reversible, mesangioproliferative lesions which are categorized as ‘class I’. Subsequent classes (II–VI) display different histopathology, more serious clinical disease, and confounding pathogenic factors. Class II lesions are encountered in patients with concomitant salmonellosis; they are typically exudative and associated with acute-onset nephrotic syndrome. Classes III (mesangiocapillary glomerulonephritis) and IV (focal segmental sclerosis) are progressive forms of glomerular disease associated with significant hepatic pathology. They are usually associated with immunoglobulin A deposits which seem to have a significant pathogenic role. Class V (amyloidosis) occurs with long-standing active infection with either S. haematobium or S. mansoni. Class VI is seen in patients with concomitant HCV infection, where the pathology is a mix of schistosomal and cryoglobulinaemic lesions, as well as amyloidosis which seems to be accelerated by the confounded pathogenesis.Early schistosomal lesions, particularly those of the lower urinary tract, respond to antiparasitic treatment. Late urological lesions may need surgery or endoscopic interventions. As a rule, glomerular lesions do not respond to treatment with the exception of class II where dual antiparasitic and antibiotic therapy is usually curative. Patients with end-stage kidney disease may constitute specific, yet not insurmountable technical and logistic problems in dialysis or transplantation. Recurrence after transplantation is rare.

AbstractSchistosomiasis is a parasitic disease that affects millions of people in 78 countries, where it is held responsible for considerable morbidity and mortality. It is caused by a blood fluke, which provokes an immunological response to hundreds of its antigens. This induces multi-organ pathology through the formation of tissue granulomata or circulating immune complexes. In addition, it is amyloidogenic and carcinogenic, through the interaction of immunological perturbation with confounding metabolic and genetic factors. The primary targets of schistosomiasis are urinary and hepatointestinal.The lower urinary tract is mainly affected in S. haematobium infection, and may lead to chronic pyelonephritis and/or obstructive nephropathy. The colon and liver are the targets of S. mansoni and S. japonicum infection, leading to hepatic fibrosis, portal hypertension, and liver failure. S. mansoni may also lead to immune complex glomerulonephritis, which is discussed elsewhere. Both S. haematobium and S. mansoni ova may be carried with the venous circulation to the lungs, where they provoke granulomatous and immune-mediated endothelial injury leading to cor-pulmonale. Ova may be subsequently carried with the arterial circulation to form ‘metastatic’ granulomas in other tissues, notably the brain (S. japonicum), spinal cord (S. haematobium), skin, conjunctiva, and genital organs.Schistosomiasis is preventable. World Health Organization programmes have successfully eradicated or reduced the incidence of infection in many countries, particularly Egypt and China. Prevention strategies include health education, raising hygiene standards, and interruption of the parasite’s life cycle by snail control and mass treatment. The search for a vaccine continues. Effective antiparasitic treatment is now possible with high elimination rates. Available agents include praziquantel and artemether for all species, metrifonate for S. haematobium, and oxamniquine for S. mansoni. Successful outcome correlates with early intervention, before fibrosis has occurred.