Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016199 (flank pain)
 2,189 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two college students who developed reversible acute deterioration in renal function following binge drinking of beer and the use of nonsteroidal antiinflammatory drugs (NSAIDs) are reported. Both patients presented with back and flank pain with muscle tenderness, but showed no evidence of overt rhabdomyolysis. The first case had marked renal failure, with a peak serum creatinine reaching 575 mumol/L (6.5 mg/dL), and acute tubular necrosis was documented by renal biopsy. The second case had only modest elevation in serum creatinine, and renal function rapidly improved on rehydration. The contribution of the potential muscle damage associated with alcohol ingestion to the changes in renal function in these two cases is not clear. However, the major mechanism for the acute renal failure was thought to be related to inhibition of renal prostaglandin synthesis in the face of compromised renal hemodynamics secondary to alcohol-induced volume depletion.
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PMID:Acute renal failure following binge drinking and nonsteroidal antiinflammatory drugs. 151 10

Cocaine abuse is associated with a constellation of serious medical complications. An unrecognized and recently described complication of cocaine use is rhabdomyolysis with acute renal failure. We describe the first patient identified in our institution with this entity, admitted to the medical services with oliguric acute renal failure. Three days prior to admission the patient had a cocaine snorting binge. He presented with bilateral flank pain, gross hematuria, vomiting and chills. No history of crush injury, prolonged immobilization and or seizures was reported. On admission the vital signs were normal, physical exam revealed periorbital edema and marked soft tissue neck swelling. Lab values: Bun 120 mgs%, Creat. 10.7 mgs%, Na 132 meq/lt, Co2 13mq/lt, Cl, 103meq/lt, Co2 13meq/lt, Ca 5.3 mgs%, CPK 30,800 U/L with a MM fraction of 98%, LDH 600 U/L, SGOT 300 U/L. The urine was dark red with a ph of 6.5 and 100 rbc/hpf. The anti-GBM antibody and blood cultures were negative. An abdominal sonogram was normal. He received peritoneal dialysis and was discharged on his 14th hospital day with a CPK of 2,800 U/L and decreasing azotemia. Cocaine associated rhabdomyolysis has only been recently described in the literature (AJM April, 88). Acute myoglobinuric renal failure needs to be added to the growing list of medical complications of cocaine use.
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PMID:Cocaine and rhabdomyolysis: report of a case and review of the literature. 207 48

All nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase, and consequently renal functions dependent upon prostaglandin synthesis can be affected. Fortunately, renal function in normal individuals is relatively independent of the PG system, and thus the NSAIDs don't usually produce any renal dysfunction. However, in some circumstances, inhibition of PG dependent renal functions can produce clinically significant effects. When the kidney is in a salt retaining state or when there is renal vascular damage, NSAIDs can reduce renal blood flow and glomerular filtration rate producing acute renal failure that is reversible upon discontinuation of the drug. NSAIDs can also: 1) reduce sodium excretion and blunt the diuretic effect of loop diuretics, thus producing or exacerbating edema, 2) inhibit PG dependent renin secretion occasionally resulting in hyperkalemia, 3) enhance the antidiuretic effects of vasopressin and 4) reduce the antihypertensive efficacy of several drugs. Evidence that any NSAID "spares" renal cyclooxygenase is controversial, and no NSAID is devoid of clinical problems. Syndromes that are less obviously related to inhibition of renal PG synthesis are acute interstitial nephritis with or without the nephrotic syndrome, renal papillary necrosis, and chronic interstitial nephritis. Recently a unique syndrome of flank pain and mild reversible renal dysfunction has been described in healthy individuals receiving suprofen, a uricosuric NSAID. This syndrome may be due to uric acid crystal deposition in the renal tubules and has resulted in the removal of suprofen from the US market.
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PMID:Renal effects of nonsteroidal anti-inflammatory drugs. 314 36

A 14 year old boy was admitted for vomiting, anorexia, flank pain and leukocyturia/hematuria. Shortly after admission, he developed anuria and acute renal failure so that hemodialysis had to be started. Pre- and post-renal causes were excluded. There were no signs of acute glomerulonephritis; liver enzymes were normal. The 123Iodine-Hippuran scan showed a shock kidney pattern lacking tubular clearance. Renal biopsy revealed an interstitial nephritis with edema and a mixed cellular infiltration. History was empty for nephrotoxic agents except for mushroom ingestion: Five days before admission the boy ate Cortinarius speciocissimus mushrooms, the toxine of which is known to be nephrotoxic, causing irreversible renal failure in severe cases (Orellanus Syndrome). Renal function did not improve much and renal transplantation was performed after 14 months on hemodialysis. In interstitial nephritis of unknown etiology the possibility of mushroom poisoning should be considered.
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PMID:[Terminal renal failure caused by interstitial nephritis following mushroom poisoning by Cortinarius speciocissimus]. 361 24

We describe a unique clinical syndrome of flank pain and acute renal failure that is associated with suprofen, a nonsteroidal anti-inflammatory drug that has recently been made available in the United States. In the initial 6 months of the drug's distribution in this country, at least 16 patients developed this syndrome. All 16 had acute flank pain and 13 developed mild reversible renal failure within 12 hours of ingestion of one to three suprofen capsules. This syndrome is unlike other nephrotoxic syndromes related to nonsteroidal anti-inflammatory drugs. The mechanism is not known.
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PMID:Suprofen-related nephrotoxicity. A distinct clinical syndrome. 380 Jan 83

An 18-year-old man with mild factor VIII deficiency developed hematuria and, subsequently, acute renal failure due to high-grade urinary obstruction by clots during therapy with cryoprecipitate, epsilon-aminocaproic acid, and acetazolamide administered for ocular trauma. Discontinuation of therapy with the latter two agents and induction of a brisk diuresis with intravenous (IV) fluid therapy resulted in return of renal function concomitant with spontaneous clot passage. A review of previous literature suggests that hemophiliacs may be more susceptible than nonhemophiliacs to high-grade urinary obstruction due to clot formation when epsilon-aminocaproic acid is administered during episodes of hematuria. Acute flank pain, fever, and delayed dense nephrograms on IV pyelogram are characteristic of the syndrome and distinguish it from other forms of acute renal failure associated with epsilon-aminocaproic acid.
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PMID:Acute renal failure due to high-grade obstruction following therapy with epsilon-aminocaproic acid. 381 74

Two cases of acute renal failure associated with ticrynafen administration are reported. Both patients had received hydrochlorothiazide prior to the institution of ticrynafen therapy and were mildly hyperuricemic. Flank pain, oliguria, and azotemia developed after the institution of ticrynafen in both cases. Clinical and laboratory features were consistent with acute uric acid nephropathy in both patients. In addition, a newly formed collection of radiolucent material was found by intravenous urography in the renal pelvis of one of the patients. Both patients were treated with intravenous fluids and sodium bicarbonate. One of the patients received allopurinol as well. Complete recovery of renal function was observed in both patients. Ticrynafen-induced hyperuricosuria in these previously volume-depleted and hyperuricemic subjects is felt to have been responsible for intrarenal and extrarenal deposition of uric acid in our patients.
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PMID:Ticrynafen-induced acute renal failure. 723 70

The binge drinking of alcohol combined with the ingestion of a nonsteroidal anti-inflammatory drug (NSAID) is a recently described cause of reversible acute renal failure. The pathogenetic mechanisms leading to acute tubular necrosis in this setting include the initial compromise in renal perfusion due to alcohol-induced extracellular volume contraction and the superimposed renal hemodynamic alterations induced by the NSAID that interfere with the renal autoregulation. Although alcohol may also cause rhabdomyolysis leading to acute tubular necrosis, this is usually not apparent in these cases. Previously, only three such cases have been reported but the incidence is likely to be higher in view of the prevalence of alcohol and NSAID use. Herein is presented another patient in whom the features of flank pain and acute renal failure in association with binge drinking and NSAID ingestion constitute a characteristic syndrome.
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PMID:Syndrome of flank pain and acute renal failure after binge drinking and nonsteroidal anti-inflammatory drug ingestion. 778 52

Acute renal failure after exercise with frank pain and patchy renal vasoconstriction is a clinical syndrome that occurs in young, previously healthy persons. The authors describe a 24-year-old man who had this syndrome. CT scan showed wedge-shaped contrast enhancement of both kidneys, which suggested patchy renal vasoconstriction. Tc-99m MDP imaging revealed diffuse increased uptake of both kidneys. After renal function was improved, Tc-99m MDP imaging showed normal uptake of both kidneys. Acute renal failure due to acute tubular necrosis was confirmed by renal biopsy. The authors conclude that Tc-99m MDP may be useful in evaluation of acute renal failure after exercise with flank pain and patchy renal vasoconstriction due to acute tubular necrosis.
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PMID:Diffuse increased renal uptake on bone scintigraphy in acute tubular necrosis. 813 77

Management of acute renal artery occlusion remains a therapeutic challenge. We report our experience with 10 cases of acute renal artery occlusion treated primarily by local infusion of fibrinolytic agents. Renal artery occlusion occurred as a result of thrombosis of a stenosed vessel in three cases, from renal artery embolism in two cases, as a complication of percutaneous transluminal angioplasty in four cases, and in association with aortic occlusion in one case. Flank pain was present in all cases and hematuria in four cases. Acute renal failure was seen at the time of presentation in four cases (one case from bilateral occlusion and three cases from an associated nonfunctioning contralateral kidney). Diagnosis was confirmed by renal isotope scanning and arteriography in all cases. All patients were treated by selective infusion of streptokinase or urokinase into the occluded renal arteries. In five cases this was combined with balloon catheter angioplasty. Therapy was initiated within 24 hours from the onset of symptoms in three cases, within 3 days in four cases, within 6 days in two cases, and after 5 weeks in one case. Successful revascularization was initially achieved in 7 of the 10 cases by arteriographic criteria. Rethrombosis occurred in one patient after 3 days and fibrinolytic therapy was repeated successfully. Renal function was restored in one of the four patients presenting with acute renal failure. One complication necessitating resection occurred as a result of fibrinolytic therapy in the form of acute mesenteric embolism with descending colon infarction. No major bleeding complications were encountered and there were no deaths in this group of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Local infusion of fibrinolytic agents for acute renal artery thromboembolism: report of ten cases. 851 15


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