Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal involvement in parasitic infections are polymorphic. Plasmodium malariae often leads to membranoproliferative glomerulonephritis whereas acute tubular necrosis or post-infectious acute glomerulonephritis are observed with Plasmodium falciparum. Urogenital taxis of Schistosoma haematobium is responsible for frequency of chronic tubular and interstitial nephritis. Without specific treatment, the renal function progressively deteriorates and urological complications appear. Schistosoma mansoni mainly leads to mesangial and membranoproliferative glomerulonephritis. Membranoproliferative and membranous glomerulonephritis are reported with loasis. Onchocerca volvulus also leads to membranoproliferative glomerulonephritis and lipoid nephrosis. Renal involvement with Wuchereria bancrofti is rare. With leishmaniosis, it is often mild but more serious observations are described: acute glomerulonephritis, nephrotic syndrome or acute interstitial nephritis. Renal hydatic cysts are diagnosed in two or three per cent of cases. Surgery is the only treatment. Immunosuppressive or antimalarial treatments seem to be ineffective in the outcome of chronic glomerulonephritis.
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PMID:[Important parasitic nephropathies: update from the recent literature]. 1022 26

Chronic kidney disease (CKD) is a major global public health problem. But kidney involvement is more common and appears more severe in Africa than in developed countries. The likely causes of end stage renal disease (ESRD) or CKD stage 3 and above in developed countries are diabetes, hypertension and less frequently glomerular diseases. In contrast, in decreasing order in Africa are glomerulopathies, hypertension and diabetes. The reasons for this preponderance of glomerular diseases are not fully known but may be linked to the persistence or reemergence of tropical diseases. This study reviews the kidney involvements more associated with common tropical diseases including HIV/AIDS. The most common HIV/AIDS lesion is a specific focal and segmental glomerulosclerosis (FSGS) termed HIV-associated nephropathy (HIV-AN). Renal complications of tropical parasites are heterogenous. Various glomerulopathies like FSGS occur during various filariasis infections. Schistosoma mansoni is responsible for membranoproliferative glomerulonephritis and amyloidosis. Human African trypanosomiasis is associated with cryoglobulinemic membranoproliferative glomerulonephritis. The Plasmodium malariae is mainly responsible for membranoproliferative glomerulonephritis. Acute patterns (acute tubular necrosis or acute postinfectious glomerulonephritis) are observed during Plasmodium falciparum infection. Several other viral, bacterial or mycobacterial infections like leprosy and tuberculosis still prevalent in Africa can also affect the kidney. Sickle cell disease is responsible for a variety of renal injuries. In conclusion, kidney lesions linked to tropical diseases partly explain the peculiar pattern of CKD of the black race and play a significant role in the current outbreak of the CKD in Subsaharan Africa.
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PMID:[Pathological peculiarities of chronic kidney disease in patient from sub-Saharan Africa. Review of data from the Democratic Republic of the Congo]. 2232 13

Many antihypertensive agents have been demonstrated to assist in preservation of kidney function, among them those that modulate calcium channels. Calcium channel blockers may also be of value in protecting hemodialysis patients from complications of sepsis. In diabetic recipients of kidney transplant allografts treated with cyclosporine, calcium channel blockade has been retrospectively linked to improved graft preservation and to fewer episodes of sepsis. This brief review outlines clinical and experimental publications on potential protection from sepsis by addition of calcium channel blockers to standard antibiotic therapy in individuals who may or may not have normal kidney function, or in the presence or absence of immunosuppression. Such mechanisms include blockade of antibiotic cytosolic extrusion in the cases of Pneumococci, Mycobacterium tuberculosis, Plasmodium falciparum malaria, or Schistosoma mansoni; blockade of the calcineurin/calmodulin pathway (in immunosuppressed patients allowing for lower dosage of cyclosporine); stabilization of calcium movement at the level of sarcoplasmic reticulum by which shock (vasopressor instability) is prevented; or of cytosolic calcium influx and cell death (in the case of allograft acute tubular necrosis). Given the high cost of development of new antibiotics, a role for generic calcium channel blockade in sepsis prevention should be pursued by additional studies to investigate potential links between blockade of calcium channels and expression of sepsis in at-risk populations.
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PMID:Does calcium channel blockade have a role in prevention of expression of sepsis in renal transplant recipients? 2792 May 69