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)

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

We recently experienced a case of renal papillary necrosis which we removed by endourological treatment. A 58-year-old female diabetic patient complaining of left flank pain, fever and chills was admitted to our clinic. She had no past history of analgesic abuse or atypical vasculitis. Physical examination revealed a body temperature of 38 degrees C and tenderness in the left costovertebral angle. Pyuria was noted, and urine cultures grew more than 100,000 colonies of Escherichia coli per cubic millimeter. DIP revealed a diminished renal function, hydronephrosis, distorted middle and lower calyces and filling defect in the dilated ureter. However, there was no evidence of obstruction or ureteral reflux. Retrograde pyelography confirmed distortion and irregularity of the calyces and hydronephrosis due to a shadow defect which was movable during radiographic examinations. Laboratory studies revealed anemia, leucocytosis and hyperglycemia, but no elevation of BUN. Therefore, the patient was diagnosed as renal papillary necrosis. We succeeded in its endourological removal through nephrostomy with a choledochoscope (Olympus Co.) under epidural anesthesia. After surgery, the patient made a satisfactory recovery.
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PMID:[Renal papillary necrosis cured with endourological treatment]. 372 27

The clinical and diagnostic features of renal papillary necrosis (RPN) of 27 patients were studied. Diabetes mellitus was the most frequent (56%) condition associated with RPN. Analgesic abuse, sickle hemoglobinopathy and urinary tract obstruction were present in 4 patients each; in 6 of these 12 patients these conditions were present as a coexistent disease with diabetes mellitus. There was evidence of an acute or chronic infection of the urinary tract in 18 patients, as a coexistent condition with another underlying disease that itself can cause RPN in 14 patients and as the only cause of RPN in another 4. Thus, the presence of more than one diagnostic condition which might be implicated in the causation of RPN was present in 15 patients or 55% of the cases in this series. When infection was excluded, six patients or 22% of the cases had two coexisting diseases, each of which has been implicated as a cause of RPN. This observation underlines the multifactorial nature of this entity and might explain why RPN is not encountered more frequently in each of the various primary diseases with which it has been associated. The average age of the patients at the time of diagnosis was 53 years for women and 56 years for men. Only six of the patients were younger than 40 years, and three of these had sickle hemoglobinopathy. The diagnosis of RPN was based on x-ray findings in eight patients, on the histologic examination of papillary tissue in urine in one, and on autopsy findings in the rest. Papillary necrosis was bilateral in three-fourths of the cases. The clinical picture varied. Most of the patients (67%) presented with chills and fever. Flank pain and dysuria were present in 11 patients (41%). As a rule oliguria was rare and progressive uremia was uncommon. In cases diagnosed at post-mortem, the patients had succumbed to infection or to a primary severe extrarenal disorder with the possibility of RPN having been entertained clinically in only half these cases prior to autopsy.
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PMID:Renal papillary necrosis: an update. 703 74

The authors present a case of a young diabetic patient with acute symptoms of pyelonephritis. The specific and permanent antibiotic treatment was ineffective and septic condition developed complicated by renal papillary necrosis. Because of the strong flank pain extensive examinations were done with negative result. The patient's condition was improving only slowly and there was need for treatment after her discharge as well. Long-term antibiotic treatment is an effective therapy to cure this previously deadly complication. Special attention should be given to diabetic patients because of frequent urinary tract infection and increased risk of renal damage among them.
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PMID:[Renal papillary necrosis in a diabetic patient]. 1132 20

The patient was a 66-year-old female who had been commonly using an analgesic for rheumatism from age 40. She visited our hospital with the complaints of fever up and right flank pain. Right hydronephrosis and renal failure were pointed out, and she was referred to the urologic clinic. Retrograde pyelography showed a clubbed upper calyx and filling defect in the lower ureter. A ureter stent was positioned for drainage in the right ureter. Then her general state improved. Three weeks later, retrograde pyelography was performed again. Two filling defects were detected in the upper ureter. Since the obstruction persisted we observed the ureter by ureteroscopy. Two specimens black-brown in color and 8 mm in diameter were observed through the ureteroscope and were removed with a basket catheter. Histological examination of the specimens revealed necrotic transepithelial tissues. It was assumed that the tissues were derived from necrotic renal papilla. Four months later, a similar episode was observed in the left upper urinary tract. The same procedures were performed to manage the patient. In this case, drainage using a ureter stent was effective and conservative therapy was possible. This is the first reported case of renal papillary necrosis managed by transurethral procedures in Japan.
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PMID:[Renal papillary necrosis managed by transurethral procedures: a case report]. 1289 30

Although the kidney is often involved in disseminated and localized candidiasis, bilateral emphysematous pyelonephritis (EPN) is infrequently reported. Renal papillary necrosis (RPN) caused by fungi is also rare. We describe a patient with bilateral RPN and EPN caused by Candida tropicalis, who suffered from recurrent hematuria, flank pain, acute fulminant renal failure, and obstruction by a sloughed papilla. He was treated successfully with antifungal therapy and percutaneous nephrostomy (PCN). This is the first case report of C. tropicalis-associated EPN and RPN.
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PMID:Candida tropicalis-associated bilateral renal papillary necrosis and emphysematous pyelonephritis. 1563 Sep 9

A 20-year-old African American male presented with a history of left flank pain and passing of light pink urine. Medical history included sickle cell trait. Urine analysis was positive for protein and blood. Metabolic profile, autoantibody screen, and complement levels were normal. Hemoglobin electrophoresis revealed an 41.8% HbS diagnostic of sickle cell trait. Creatinine clearance was normal and proteinuria was nonnephrotic. A noncontrast computed tomography (CT) scan showed left proximal hydronephrosis. Urology follow-up was arranged and the differential included renal papillary necrosis, or renal cyst rupture. He presented 3 months later with sudden onset left flank pain and gross hematuria. Serum creatinine was 1.8 mg/dL. Computed tomography scan with contrast revealed innumerable lung lesions, an enlarged heterogenously enhancing left kidney, and retroperitoneal adenopathy. Ultrasound revealed an obstructed left collecting system and a 14-cm enlarged left kidney with no discrete mass. Testicular markers/ultrasound, upper/lower endoscopies were normal. Lung biopsy revealed poorly differentiated adenocarcinoma positive for cytokeratin 7. Renal, sarcoma, and gastrointestinal markers were negative. By exclusion, it appeared that the patient had a carcinoma of unknown primary. However, with the clinical and personal history, a diagnosis of renal medullary carcinoma (RMC) was made. RMC is a rare and highly malignant tumor that should always be included in the differential of a patient with sickle cell disorder and hematuria. Renal biopsy typically fails to sample the renal medulla and radiologic findings might not raise the suspicion of a renal tumor. Thus, clinical suspicion must always be high in order to preserve the patient's only chance of prolonged survival.
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PMID:Adenocarcinoma of unknown primary in a 20-year-old African American male. 1969 25

Diabetes mellitus (DM) is a common disease in Oman as in rest of Gulf Cooperation Council where metabolic syndrome is of high prevalence. DM is a foremost risk factor for urinary tract infections (UTIs). It is also linked to more complicated infections such as emphysematous pyelonephritis (EPN), emphysematous pyelitis (EP), renal/perirenal abscess, emphysematous cystitis, xanthogranulomatous pyelonephritis, and renal papillary necrosis. The diagnosis of these cases is frequently delayed because the clinical manifestations are generic and not different from the typical triad of upper UTI, which include fever, flank pain, and pyuria. A middle-aged female with DM and chronic kidney disease stage IV was admitted with recurrent UTI with extended-spectrum beta-lactamase-producing Escherichia coli. At presentation, she was afebrile, clinically stable, had no flank pain and there was no leukocytosis. Laboratory test for C- reactive protein done twice and was only mildly elevated at 7 and 11 mg/dL. A computed tomography scan of kidney-ureter-bladder (CT-KUB) was recommended and reported as "no KUB stone but small atrophic left kidney with dilatation of the pelvicalycial system and ureter and the presence of air in the collecting system suggestive of EP." Thus, commonly associated with DM, especially in females, debilitated immune-deficient individuals, and patients harboring obstructed urinary system with infective nidus. Air in the kidney is not always due to EPN. UTI with a gas-producing organism can ascend to the kidney in the presence of vesicoureteral reflux.
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PMID:Gas in the kidney in asymptomatic Escherichia coli urinary tract infections in a patient with severe vesicoureteral reflex. 3124 37