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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although haematuria is a relatively common symptom of hemophilia A and B, renal disease seemed to be a rarity and it has usually been held that this symptom was benign in nature. However detailed studies of renal function in a series of such patients using radiological and biochemical tests of renal function show significant differences compared to normal. These abnormalities seem to be associated with recurrent haematuria but do not appear to be related directly to replacement therapy with plasma concentrate and do not occur more frequently in patients who have received long term fibrinolytic inhibitors. Other rare renal disorders associated with haemophilia include nephrotic syndrome, trauma, acute tubular necrosis, analgesic nephropathy and chronic pyelonephritis.
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PMID:Renal disorders in haemophilia A and B. 26 97

Acute, usually reversible, renal failure has been observed in patients with normal or minimally altered glomeruli on renal biopsy. This review aims to examine the clinical features of acute renal failure in these patients and to evaluate factors that may contribute to the reduction in glomerular filtration rate (GFR). In an analysis of 79 cases affecting 75 patients reported in the English literature since 1966, with acute renal failure associated with minimal change disease or mild histopathological changes in glomeruli, the average age was 58 +/- 2 years (mean +/- 5 SEM), urine protein excretion 11.6 +/- 0.6 g/d, and serum albumin level 19 +/- 1 g/L (1.9 +/- 0.1 g/dL). Acute renal failure was documented an average of 29 +/- 5 days after onset of nephrotic syndrome, and persisted for 7 weeks in 62 episodes in the 58 patients in whom recovery of renal function occurred. Fourteen patients died of uremia or required chronic dialysis, and 3 were lost to follow-up. Although plasma volume depletion was sometimes cited as the cause of renal failure, objective signs of hypovolemia were not documented and most patients did not improve after treatment designed to correct volume deficits. In contrast, histopathological changes consistent with acute tubular necrosis (ATN) were observed in at least 60% of cases. Since the pathogenesis of acute renal failure in minimal change nephrotic syndrome is unknown, we evaluated hemodynamic determinants of GFR in patients with minimal change disease with normal or near-normal renal function, and in relevant animal models, to obtain insights into the effect of nephrotic syndrome on GFR. Although acute renal failure is uncommon, GFR is reduced concurrently with nephrotic syndrome in approximately 30% of children and adults. Absolute and effective blood volume and renal plasma flow are relatively well preserved. However, clinical and experimental observations suggest that the glomerular ultrafiltration coefficient may be reduced by as much as 50%. These findings, together with renal biopsy changes in cases with acute renal failure, suggest that severe reductions in GFR in some patients with minimal change nephrotic syndrome may result from an interaction between acute ischemic tissue injury and preexisting intrinsic renal abnormalities.
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PMID:Reversible renal failure in the nephrotic syndrome. 155 65

Azotemia and diabetes mellitus are now well-known adverse reactions associated with Pentamidine treatment, especially since its prescription in case of Pneumocystis carinii pneumonia. We report the case of a 2 year-old boy, treated for kala-azar with pentamidine and N-methyl glucamine antimoniate who developed adverse effects, characterized by a nephrotic syndrome associated with the classic acute tubular necrosis, and transient diabetes mellitus.
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PMID:[Transitory acute kidney insufficiency and insulin-dependent after treatment of kala-azar with pentamidine and N-methylglucamine antimony]. 185 38

The urinary sediment was examined by light microscopy in 65 consecutive inpatients with renal insufficiency (not due to pre- or postrenal factors) referred to a nephrology consult service for evaluation. In the 60 patients in whom a single diagnosis was reached, the sediments of 34 (57%) contained an easily recognized cell, which we have called the "bubble cell". These cells were bizarre, large cells with a single nucleus, which appeared to contain one or more fluid-filled vesicles. Bubble cells were most prevalent in the sediment of patients with acute tubular necrosis but were also seen a variety of other renal diseases. In most patients with acute tubular necrosis, the sediment also contained "normal"-appearing renal tubular cells, muddy brown casts, and oval fat bodies which were indistinguishable from those seen in the nephrotic syndrome. By electron microscopy, the bubble cells appeared to be vacuolated renal tubular epithelial cells, which had characteristics of viable cells. Most bubble cells excluded the vital dye Trypan blue, whereas the normal-appearing renal tubular cells were typically strongly positive. It was concluded that bubble cells, often accompanied by oval fat bodies, are commonly present in the sediment of patients with acute tubular necrosis as well as many other types of renal disease. Most cells which would be classified as "normal" renal tubular cells in these sediments are dead. In contrast, the findings suggest that the bubble cell represents an injured but viable renal tubular cell. The frequent finding of oval fat bodies in the same sediments suggests that the oval fat body is also produced by tubular cell injury.
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PMID:Bubble cells: renal tubular cells in the urinary sediment with characteristics of viability. 188 70

There is a growing number of hospitalised patients who develop a drug-induced renal problem because increasing numbers of potent drugs have been added to the therapeutic arsenal in recent years. The 3 clinical syndromes that can be recognised in drug-induced nephropathy are acute renal failure, chronic interstitial nephritis and the nephrotic syndrome. The first can be caused by prerenal problems, acute interstitial nephritis, acute tubular necrosis and intratubular obstruction. The most important drugs that cause prerenal failure are NSAIDs, captopril and cyclosporin. NSAIDs inhibit the synthesis of prostaglandins, and consequently vasoconstriction of the afferent arteriole leads to lowering of the glomerular filtration rate (GFR); captopril blocks the formation of angiotensin II (which also leads to a lower GFR), and should be used with caution in patients with stenotic renal arteries; cyclosporin causes vasoconstriction of the afferent arteriole, which is probably mediated by the sympathetic system. Combinations of these drugs result in increased nephrotoxicity. The drugs most likely to cause acute interstitial nephritis are antibiotics and NSAIDs. Normally, signs of an allergic reaction are also present. Acute interstitial nephritis is usually self-limiting, but in some studies it is claimed that steroids may promote recovery. Four important causal agents of acute tubular necrosis are aminoglycosides, amphotericin B, radiocontrast agents and cyclosporin. Approximately half of the cases of drug-induced renal failure are related to the use of aminoglycosides: generally, 10 days after start of treatment a nonoliguric renal failure develops, with recovery after withdrawal of the drug in almost all cases. The aminoglycosides are particularly nephrotoxic when combined with other nephrotoxic drugs. 80% of amphotericin B-treated patients develop renal insufficiency, a percentage that increases as the cumulative dose exceeds 5g. It is because of its unique antifungal properties that there are still some indications for the use of this highly nephrotoxic drug; the high percentage of nephrotoxicity can probably be prevented in part by sodium loading. The nephrotoxicity of radiocontrast agents is largely dependent on renal function: from 0.6% in patients with normal renal function to 100% in patients with a serum creatinine above 400 mumol/L. Diabetes mellitus does not add greatly to the risk of radiocontrast nephrotoxicity. The nephrotoxicity of cyclosporin is dose-dependent and reversible, although there are some reports of irreversibility after long term use. Cyclosporin can also result in nephrotoxicity in combination therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Drug-induced nephrotoxicity. Aetiology, clinical features and management. 204 84

This report concerns two boys with minimal change nephrotic syndrome progressed to renal failure. The first case aged 17 being a steroid sensitive infrequent relapse developed acute renal failure at his third relapse and recovered soon after the treatment with diuretics and corticosteroids. The second case aged 15 being a steroid dependent frequent relapse became steroid resistant at his 11th relapse and progressed to renal failure seven months later. As the causes of renal failure, acute tubular necrosis and tubular obstruction by casts were suspected in the former. Renal vein thrombosis, morphological transition of renal histology, hemodynamic change and change in glomerular permeability might be occurred in the latter. Renal failure is a rare complication of minimal change nephrotic syndrome and the cause is variable. Precise diagnosis and prompt treatment should be needed to improve the prognosis.
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PMID:[Rapid deterioration of renal function in minimal change nephrotic syndrome]. 205 45

Reported was an aged woman (80-year-old) of minimal change nephrotic syndrome which was complicated with reversible oliguric acute renal failure. The patient presented massive proteinuria, anasarca, and severe azotemia. She recovered conservatively from the acute renal failure and subsequently remitted from the nephrotic syndrome after the treatment which comprised albumin infusion, diuretics, adrenocorticosteroid hormones (including the pulse therapy), antiplatelet drug, and anticoagulants. The histopathologic findings of renal biopsy were compatible with minor glomerular abnormalities and acute tubular necrosis with many tubular casts. The previously reported cases older than 80-year-old which remitted from minimal change nephrotic syndrome complicated with reversible acute renal failure, were very rare. The present case was the second case among the literatures.
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PMID:[An aged woman with minimal change nephrotic syndrome complicated with reversible acute renal failure]. 219 Nov 62

A previously healthy 29-year-old homosexual man presented with a 4-day history of fever, malaise, sore throat, and bleeding gums. Rhabdomyolysis, acute renal failure, and nephrotic range proteinuria were also present. The patient was found to have acute human immunodeficiency virus (HIV) infection confirmed by the presence of HIV antigen in his serum and subsequent evolution of an HIV antibody profile typical of acute seroconversion. A kidney biopsy revealed acute tubular necrosis and mesangioproliferative glomerulonephritis, with tubuloreticular inclusions. In the presence of otherwise unexplained acute renal failure, rhabdomyolysis, or new onset nephrotic syndrome, acute HIV infection should be considered in the differential diagnosis.
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PMID:Acute human immunodeficiency virus infection temporally associated with rhabdomyolysis, acute renal failure, and nephrosis. 233 Apr 81

Renal involvement in Hansen's disease was evaluated in 94 Portuguese patients, average age and duration of disease of 47.6 and 6.8 years respectively. Sixty-seven were studied retrospectively and 27 prospectively; renal biopsy was obtained in 4, fat-tissue needle aspiration for amyloidosis in 20, and tubular function was tested in ten. Mild proteinuria and/or haematuria was found in 33 patients, the severity increasing during erythema nodosum leprosum reactions, but without overt nephritic or nephrotic syndrome. Two patients had renal amyloidosis on biopsy and two more were confirmed by fat biopsy, a 10.5% incidence in those studied prospectively; all but one were of the lepromatous type, with frequent bouts of erythema nodosum leprosum. The two other renal biopsies showed mesangial glomerulonephritis, and one unexplained acute tubular necrosis; none had immune deposits by immunofluorescence. Proximal acidification was always normal, distal acidification tested by bicarbonate infusion was abnormal in one of nine patients, and six of nine patients had concentration defects. Leprosy causes frequent urinary sediment changes and concentration defects, usually without clinical expression; proteinuria and/or glomerular involvement is mainly due to amyloidosis.
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PMID:Renal involvement in leprosy. 249 59

In the past 15 years, there has been an explosion in the number of nonsteroidal anti-inflammatory drugs on the market. Along with this explosion have come increasing reports of the physiologic and pathologic changes seen in the kidneys. This report reviews the effects of prostaglandins on the kidney and the physiologic changes that result when prostaglandin synthesis is blocked. The world literature on renal complications of nonsteroidal anti-inflammatory drugs is reviewed and 274 cases of acute renal disease associated with their use are reported. The following cases are described: nephrotic syndrome (34); acute interstitial nephritis (51); acute tubular necrosis (29); papillary necrosis (53); poor perfusion with renal failure (40); acute glomerulitis or vasculitis (13); and unspecified renal failure (102). Fenoprofen appeared to be more nephrotoxic than other nonsteroidal anti-inflammatory drugs and resulted in multiple renal lesions in the same patient.
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PMID:Effects of nonsteroidal anti-inflammatory drugs on prostaglandins and renal function. 286 41


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