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)

A review of 85 patients aged 60 years or more, treated in a southern Indian hospital for conditions requiring renal biopsy, showed that diffuse poliferative glomerulonephritis was the most frequent diagnosis, being present in 24 cases of whom 11 had elevated serum streptococcal antibody titres. Infections were also important in 2 patients with amyloidosis secondary to tuberculosis, in 3 patients with acute tubular necrosis following infectious gastroenteritis and in a patient with acute pyaemic interstitial nephritis with septicaemia. Drugs including indigenous medicines were the other important cause of renal disease, being implicated in 11 cases.
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PMID:Medical renal disease in the elderly in a southern Indian hospital. 338 Feb 27

Nephrotic syndrome was the commonest clinical presentation among 2827 consecutive adult Indian patients from whom adequate kidney biopsies were obtained for suspected renal disease. In 83 per cent of cases the nephrotic syndrome was due to minimal change disease, focal segmental glomerulosclerosis, mesangiocapillary glomerulonephritis, membranous usually secondary to tuberculosis or leprosy, was present in only 34 patients. Acute nephritis, the next most frequent clinical presentation, was due to diffuse endocapillary proliferative, crescentic or mesangial proliferative glomerulonephritis in 88 per cent of cases, almost half of whom had elevated serum streptococcal antibody titres. Eosinophilia showed a highly significant association with diffuse endocapillary proliferative and mesangiocapillary glomerulonephritis. Idiopathic IgA nephropathy was present in only 10, and antiglomerular basement membrane antibody disease in only one, of the 238 patients whose biopsies were studied by immunofluorescence. Complications of pregnancy accounted for 70 per cent of cases of cortical necrosis. Acute gastroenteritis, septicaemia, abortions, snake bite and allopathic and indigenous medicines were important causes of acute tubular necrosis.
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PMID:Renal disease in adult Indians: a clinicopathological study of 2,827 patients. 344 84

The early use of gold in medicine and dentistry dates back to the ancient Chinese and Egyptians. The discovery in 1890 that gold salts were toxic in vitro to tubercle bacilli led to the extensive treatment of tuberculosis with gold salts in the first three decades of this century. Eventually, gold therapy was extended to arthritis and lupus erythematosus, because of the belief that these diseases were forms of tuberculosis. Because of its beneficial effect particularly on active rheumatoid arthritis, chrysotherapy has remained one of the most widely used treatments of rheumatoid arthritis for the past half century. Toxicity of gold salts includes hypersensitivity reaction of skin and mucous membranes, bone marrow depression, and nephrotoxicity. The nephrotoxic clinical manifestations are renal insufficiency, proteinuria and hematuria, and the nephrotic syndrome. The pathologic changes are tubular degeneration, acute tubular necrosis or immune complex glomerulonephritis. The justification that any of these possible changes are the result of gold therapy rests clinically upon the time relationship of gold therapy and the renal symptoms, and pathologically upon the presence of gold inclusions (aurosomes) in proximal tubular epithelial cells. Aurosomes can at times be visualized by light microscopy, are usually seen by electron microscopy, and can be identified by microprobe analysis. Their pathology will be illustrated and pathogenic mechanisms discussed.
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PMID:Gold nephropathy. 703 39

Renal biopsies of 43 patients who developed renal complications after treatment with antibiotics were studied. The treatment with antibiotics in these cases was used for many different reasons such as: bronchitis, bronchopneumonia, cystitis, tonsillitis, sepsis, peritonitis, gangrene of the foot and tuberculosis. The renal function of these patients, before the treatment with antibiotics was normal. The biopsies were studied by light, electron and immunofluorescence microscopy. In 43 cases treated with antibiotics renal changes were shown. Three types of morphologic changes were found: acute tubular necrosis (ATN) (13 cases), acute tubulo-interstitial diseases (ATID) (21 cases), focal glomerulonephritis with crescents (FGN) (9 cases). The renal pathologic changes were most commonly seen in patients treated with 2 groups of antibiotics: aminoglycosides (21 cases) and antibiotics of the penicillin group (15 cases). The most characteristic feature of aminoglycosides is their direct toxic effect leading to ATN. Antibiotics of the penicillin type more commonly caused an allergic reaction leading to ATID (secondary to cellular mechanisms) or FGN (secondary to a predominantly humoral mechanism). Renal changes in the use of other antibiotics were much less manifest and were usually due to a hypersensitivity reaction. Cephalosporins, if used in combination with other antibiotics can increase their nephrotoxicity.
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PMID:Antibiotic associated nephropathy. 870 64

Nephropathy as the sequences of Hansen's disease before and after the introduction of chemotherapy was compared referring to the report by Hayashi in 1943 and the summary of the autopsy reports from 1978 to 1981 at National Hansen's disease hospital Zenseien. Unlike the high rates of tuberculosis as the cause of death before the introduction of chemotherapy (41.3%) those thereafter decreased to be negligible. On the other hand the comparison of the rates of nephropathy with the same way as that of tuberculosis was impossible since the description about nephropathy by Hayashi was not sufficient to characterize each nephropathy since he included arteriolitis, glomerulonephritis and interstitial nephritis together in the term of nephritis. Death rate due to nephritis among Hansen's disease patients according to Hayashi at that time was 21.2% which was twice as many comparing to that in the other cases. According to the report about the cases of Zenseien those reported to have glomerulonephritis was 37.3% though those were not necessarily listed as the cause of death. Also the nephropathy including fibrinoid angitis with occasional microaneurysmal dilatation of afferent arteries, glomerulitis, sclerosis and stricture of efferent arteries likewise ischemic acute tubular necrosis possibly as the result of these angiopathy seemed to be present. These vascular changes partially resemble to that of microscopic periarteritis nodosa but seems to be common in the smaller arteries. In conclusion, unlike the case of tuberculosis the rate of nephritis including glomerulitis, arteriolitis and interstitial nephritis as Hayashi used as his criteria does not seem to have decreased. Therefore, the critical analysis of the nephropathy especially of that relating to the arteriolitis should be done to obtain the knowledge to suppress its occurrence.
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PMID:[Hansen's disease and nephropathy as its sequence]. 930 Dec 9

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

Rifampin-induced acute kidney injury is very rare. Most cases of acute renal injury from rifampin use are related to acute tubular necrosis and acute interstitial nephritis. In this case report, we detail a unique presentation of rifampin-associated acute intravascular hemolysis and subsequent tubular injury in a tuberculosis patient. The patient had presented to the hospital with acute kidney injury and oliguria from intravascular volume depletion secondary to intractable vomiting. The patient had stopped taking his antituberculosis medications two weeks before hospitalization. At the time of hospital admission, his antituberculosis regimen of rifampin and isoniazid was reinstituted. Within four days of initiation of rifampin, he developed acute hemolytic anemia. His kidney biopsy revealed hemoglobin pigment deposition in the kidney tubules. Rifampin was discontinued, and he received a total of eight hemodialysis treatments spanning over 17 days. Subsequently, after discontinuing rifampin, his anemia and oliguria resolved with renal function markedly improved to near normal baseline levels. This case report also offers a review of known mechanisms of rifampin-induced acute hemolysis and acute renal failure, along with a discussion of contemporary literature.
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PMID:Rifampin-Induced Acute Intravascular Hemolysis Leading to Heme Pigment-Related Kidney Injury. 3278 61