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

Selective cyclooxygenase-2 (COX-2) inhibitors are relatively newer anti-inflammatory drugs that produce comparable antiinflammatory and analgesic effects to the nonselective nonsteroidal antiinflammatory drugs (NSAIDs); but with fewer symptomatic gastric and duodenal ulcers. Limited data are available concerning the toxicity associated with COX-2 inhibitors outside the gastrointestinal tract. The NSAIDs have been known for their nephrotoxic potentials including minimal-change disease (MCD) with interstitial nephritis. Although the recent data suggests that COX-2 inhibitors may have the same adverse renal effect as NSAIDs, there is only one case report describing minimal change disease and acute interstitial nephritis (AIN) associated with a COX-2 inhibitor, celecoxib. We are reporting a case of MCD and acute tubular necrosis (ATN) but without interstitial nephritis in a patient treated with celecoxib. Although the proteinuria in our patient resolved completely after discontinuation of celecoxib, the renal function did not. We suggest that heightened suspicion of this side effect of COX-2 inhibitors should be maintained in all patients taking this class of drugs who present with nephrotic syndrome.
 ...
PMID:Cyclooxygenase-2 inhibitor-associated minimal-change disease. 1590 98

The most frequent causes of glomerular diseases whose main clinical syndrome are nephrotic syndrome and acute renal failure may have several causes: acute tubular necrosis, thrombosis of renal veins, acute tubulointerstitial nephritis. Infrequently, the association between primary glomerular disease (membranous nephropathy and others) and crescentic glomerulonephritis can cause this clinical picture. We describe a young woman without systemic disease with nephrotic syndrome and acute renal failure secondary to membranous nephropathy and superimposed crescentic glomerulonephritis. She received steroids and cyclophosphamide with stabilization of renal function after two months of follow-up.
 ...
PMID:[Membranous nephropathy and crescentic glomerulonephritis]. 1605 15

Hemophagocytic syndrome (HPS) is defined by bone marrow and organ infiltration by activated, nonmalignant macrophages, which phagocytose blood cells. The clinical spectrum of HPS is broad, but renal involvement has rarely been investigated. We report a previously unknown renal manifestation of HPS: nephrotic syndrome. This multicentric retrospective study included patients fulfilling the following criteria: (i) no history of nephropathy; (ii) HPS diagnosis with histologic evidence of hemophagocytosis; (iii) occurrence of nephrotic syndrome during HPS; and (iv) available renal histology. Using the same criteria, we also searched the literature for additional cases. We identified nine patients retrospectively and found two additional cases in the literature (five males and six females, whose mean age was 34 +/- 27 years). Black African patients predominated (63.6%). HPS was due to lymphoma (six cases), infectious disease (three cases), and autoimmune disease (one case), and was primary in one patient. Acute renal failure was associated with nephrotic syndrome in 10/11 cases. Renal histology showed acute tubular necrosis associated with collapsing glomerulopathy in five patients (all Africans with negative human immunodeficiency virus serology), minimal change glomerulopathy in four, and thrombotic-microangiopathy with abnormal podocytes in two. Death occurred in seven cases. Nephrotic syndrome should be included among the renal complications of HPS with acute renal failure. We postulate that abnormal T-cell activation and/or high pro-inflammatory cytokine levels during HPS might cause podocyte injuries, especially among African patients with a susceptible genetic background.
 ...
PMID:Nephrotic syndrome associated with hemophagocytic syndrome. 1655 22

IgA nephropathy (IgAN) is an important cause of progressive kidney disease with 25-30% of patients developing end-stage renal disease within 20 years of diagnosis. There is still no treatment to modify mesangial IgA deposition and available treatments are those extrapolated from the management of other patterns of chronic glomerulonephritis. There remains no consensus on the use of immunosuppressive agents for treatment of progressive IgAN and this is compounded by the relative lack in IgAN of randomized controlled trials relevant to current clinical practice. Patients with recurrent macroscopic hematuria or isolated microscopic hematuria and proteinuria <1 g/24 h require no specific treatment. Those with nephrotic syndrome and minimal change on renal biopsy should be managed as for minimal change nephropathy. There is no evidence to support the use of corticosteroids for nephrotic IgAN outside this group of patients. Patients presenting with acute renal failure require evaluation to distinguish acute tubular necrosis, which requires supportive therapy only, from crescentic IgAN, for which treatment with cyclophosphamide and corticosteroids in a regimen similar to that for renal small vessel vasculitis is indicated in the absence of significant chronic histologic injury. Patients at greatest risk of progressive renal impairment are those with hypertension, proteinuria >1 g/24 h, and reduced glomerular filtration rate at diagnosis. All such patients should be treated to a blood pressure of 125/75 mm Hg with dual blockade of the renin-angiotensin system with angiotensin-converting enzyme inhibition and angiotensin receptor blockade. At present, there is insufficient evidence for the additional use of immunosuppressive agents, antiplatelet agents, or anticoagulants.
 ...
PMID:Treatment of IgA nephropathy. 1705 Dec 61

We report a 19-year-old Saudi female with nephrotic syndrome whose renal biopsy revealed findings suggestive of minimal change glomerulonephritis (MCGN). She developed oliguric renal failure requiring hemodialysis. She remained dialysis dependent for five weeks and subsequently renal function recovered fully. She remained nephrotic and responded to a six week course of corticosteroids. She was followed for two years during which she had two relapses, which responded to steroids. Acute renal failure is uncommon in MCGN and is due to acute tubular necrosis induced by hypovolemia or drugs. This patient did not have any obvious precipitating factor, which led to acute reversible renal failure.
 ...
PMID:Idiopathic reversible renal failure in a young woman with minimal change glomerulonephritis. 1690 27

Renal dysfunction and injury secondary to medications are common, and can present as subtle injury and/or overt renal failure. Some drugs perturb renal perfusion and induce loss of filtration capacity. Others directly injure vascular, tubular, glomerular and interstitial cells, such that specific loss of renal function leads to clinical findings, including microangiopathy, Fanconi syndrome, acute tubular necrosis, acute interstitial nephritis, nephrotic syndrome, obstruction, nephrogenic diabetes insipidus, electrolyte abnormalities and chronic renal failure. Understanding the mechanisms involved, and recognizing the clinical presentations of renal dysfunction arising from use of commonly prescribed medications, are important if injury is to be detected early and prevented. This article reviews the clinical features and basic processes underlying renal injury related to the use of common drugs.
 ...
PMID:Drug-associated renal dysfunction and injury. 1693 99

The chemokine SDF-1alpha is involved in migration, survival, and development of multiple cells, most notably of hematopoietic stem cells (HSC) expressing its ligand CXCR4. Recently, we have shown engraftment of human HSC in the ischemically injured murine kidney, presumably mediated by SDF-1alpha. To further investigate a possible role of SDF-1alpha in the recruitment of CXCR4(+) cells in human renal disease of varying etiologies, we immunostained human biopsies of immunoglobulin (Ig)A nephropathy, minimal-change nephrotic syndrome, focal segmental glomerulosclerosis, membranoproliferative glomerulonephritis, chronic pyelonephritis, and acute tubular necrosis (ATN) for SDF-1alpha, CXCR4, and CD45, a pan-hematopoietic marker. Irrespective of the diagnosis, intense SDF-1alpha immunoreactivity was localized to distal tubules and collecting ducts, whereas CXCR4 showed intense staining in both distal and proximal tubules. In addition, whereas varying degrees of CD45(+) cell infiltrates were observed in all biopsies, we found focal infiltrates of CXCR4(+) cells mostly localized to the corticomedullary junction only in ischemic ATN. This correlated with more extensive staining for SDF-1alpha in these sites. In all investigated renopathologic conditions, CD45+ leukocyte recruitment to the kidney seems not to be driven by SDF-1alpha/CXCR4 interaction. A contribution of SDF-1alpha for influx of CXCR4(+) cells in the vicinity of arcuate vessels is suggested only in human ATN.
 ...
PMID:Expression of SDF-1/CXCR4 in injured human kidneys. 1797 9

Nephrotic syndrome is infrequently complicated with appearance of acute renal failure and minimal change disease is the glomerulopathy more usually involved. Pathogenesis is unclear and three possible mechanisms it has been proposed to explain the decrease of glomerular filtration rate: a severe reduction of glomerular permeability, the presence of acute tubular necrosis or an increased intrarenal pressure related with interstitial oedema. Here we present a 36 years-old-male with a nephrotic syndrome caused by focal and segmental glomerulosclerosis who developed an anuric acute renal failure. Renal function did not change despite oedema removal with haemodialysis and only after corticosteroid and cyclophosphamide therapy introduction we observed a rapid recovery of urinary output and resolution of acute renal failure. Renal biopsy did not show signs of tubular damage or obstruction with proteins nor significant interstitial oedema. Therefore, in this case we think acute renal failure was caused by a severe reduction in glomerular ultrafiltration rate and steroids were the effective treatment that allowed recovery of renal function.
 ...
PMID:[Acute renal failure in a case of nephrotic syndrome secondary to focal and segmental glomerulosclerosis]. 1833 41

Insulinlike growth factor I (IGF-I), IGF-I receptors, and IGF-binding proteins are expressed in different segments of the nephron in a relationship that suggests autocrine, paracrine, and endocrine modes of action. IGF-I contributes to compensatory nephron growth in a variety of experimental renal diseases with loss in functioning nephron number, and to tissue repair after ischemic acute tubular necrosis. IGF-I causes arteriolar dilatation in the kidney and increases the glomerular filtration rate in experimental animals, in normal subjects, as well as in patients with chronic renal failure, and this effect of the peptide is probably mediated by nitric oxide. IGF-I raises proximal tubular phosphate reabsorption and may increase sodium absorption in distal tubules. In the nephrotic syndrome, IGF-I- and IGF-binding protein complexes are excreted in urine and IGFBP-3 protease activity is increased, causing complex abnormalities in the IGF-system.
 ...
PMID:Insulinlike growth factor I and the kidney. 1840 31

We describe a patient who developed renal failure during antituberculous therapy. The condition was characterized by an initial phase of acute tubular necrosis and nephrotic syndrome which ultimately progressed to end-stage renal disease with severe interstitial fibrosis, despite adequate period of drug withdrawal. At that time, tuberculous infection was inactive and there was no evidence of amyloidosis or renal vein thrombosis.
 ...
PMID:Progressive interstitial fibrosis and nephrotic syndrome associated with antituberculous therapy. 1858 41


<< Previous 1 2 3 4 5 6 7 8 Next >>