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)

We are reporting the first case, to our knowledge, of a venous embolus to a transplanted kidney. The embolus occurred five days after transplantation of a cadaver kidney in a 31-year-old woman who was receiving estrogen-progesterone therapy for menorrhagia. Five hours after acute onset of left flank pain and anuria, the embolus was identified at the anastomosis of the donor renal vein to the external iliac vein. The embolus was manipulated distally in the external iliac vein and excluded by proximal division of the vein. Recovery was eventually complete, despite two major postoperative complications, acute tubular necrosis and a perirenal hematoma secondary to heparin sodium therapy. Radionuclide scanning was critically important in establishing the diagnosis and in assessing the potential for the kidney to recover from acute tubular necrosis. On the basis of this experience, we believe that prompt surgical intervention is indicated for acute venous occlusion.
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PMID:Venous embolus to a transplanted kidney. Diagnosis and treatment. 78 79

Experience with chemodissolution of uric acid stones in 30 patients is presented. Chemodissolution was achieved either with infusion of 0.16 M i.v. lactate or oral sodium bicarbonate, in addition to liberal fluid intake and allopurinol wherever indicated. In some cases direct chemodissolution by in situ irrigation with sodium bicarbonate solution was done after an initial percutaneous nephrostomy. Seven patients presented with acute obstructive anuria. In this group, 5 of them had bilateral obstructive calculi, while 2 had unilateral obstruction in a solitary kidney. The latter 2 had complete recovery following intravenous lactate therapy. Of the 5 presenting with bilateral obstruction, 2 patients had complete response to chemodissolution, whereas the remaining 3 had only a partial response requiring surgery for ultimate salvage. In this group I, 6 patients are doing well with a normal serum creatinine at 3 months to 4 years follow-up, while 1 patient has a serum creatinine, stabilised at 3.2 mg%. In the second group, 23 patients presented with non-obstructing urinary stones. Flank pain was the commonest complaint and a concomitant history of gout was present in 6 patients. Hyperuricaemia was detected in 12 and hyperuricosuria in 19. All cases were managed by high fluid intake and oral sodium bicarbonate, with self-monitoring of urine pH, which was kept between 6.5 and 7.0. Allopurinol was administered in cases having hyperuricaemia and/or hyperuricosuria. Systemic alkali therapy in the form of intravenous molar lactate or sodium bicarbonate is effective and safe both in obstructive anuria and non-obstructive urinary uric acid stones.
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PMID:Chemodissolution of urinary uric acid stones by alkali therapy. 131 80

A 62-year-old man with pneumonia and left flank pain had a clinical syndrome of hyponatremia, hypotension, dehydration, and high urinary sodium excretion in the presence of a normal glomerular filtration rate. The plasma level of antidiuretic hormone was relatively high despite decreased serum osmolality. Thyroid function and excretion of glucocorticoid and sex steroids were normal. The serum aldosterone level was very low despite elevated plasma renin activity. Angiotensin II failed to stimulate any secretion of aldosterone, despite the occurrence of a progressive rise in blood pressure. On the other hand, rapid ACTH administration increased both serum aldosterone and cortisol. The patient showed no effective response to increased salt intake, but large doses of mineralocorticoid resulted in a normal serum sodium level without dehydration. Subsequently, he suffered cardiac arrest secondary to ventricular tachycardia. Postmortem examination showed well differentiated adenocarcinoma in the left pleura and an intact, histologically normal adrenal zona glomerulosa and kidney. This is the first reported case of a critically ill patient with hyponatremia caused by hyperreninemic hypoaldosteronism possibly due to angiotensin II insensitivity and tubular unresponsiveness to mineralocorticoid.
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PMID:Hyponatremia and hyperreninemic hypoaldosteronism in a critically ill patient: combination of insensitivity to angiotensin II and tubular unresponsiveness to mineralocorticoid. 217 79

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

Suprofen, a nonsteroidal anti-inflammatory drug, has been associated with the onset of acute flank pain, hematuria, and transient renal dysfunction after the ingestion of one or two doses, particularly in young males. Potential mechanisms of this nephropathy were evaluated in normal males following ingestion of suprofen (200 mg) on two occasions: the first with ad libitum fluid intake and the second during forced water diuresis. On the first study occasion, creatinine clearance, the fractional excretions of uric acid (FEUA) and sodium (FENa), the urinary concentration of undissociated uric acid, and the urinary excretions of prostaglandins and glomerular and tubular proteins were assessed. On the second occasion, inulin and PAH clearances and FEUA and FENa were determined. Within 90 min after suprofen administration, the FEUA increased from 8.8 +/- 2.6 to 35.5 +/- 9.6% (p less than 0.05). Urine became supersaturated for uric acid during ad libitum fluid intake. Glomerular filtration rate, renal plasma flow, and FENa decreased significantly, while prostaglandin and protein excretions did not change. The findings are consistent with acute uric acid nephropathy as a mechanism of suprofen-induced renal dysfunction.
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PMID:Suprofen-induced uricosuria. A potential mechanism for acute nephropathy and flank pain. 339 26

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

A 26-year-old female visited our hospital complaining left flank pain and macroscopic hematuria. She had been suffering ulcerative colitis and administered salazosulphapyridine and predonisolone from 17-year-old. Intravenous urography showed radiolucent multiple stones in the left renal pelvis. Three sessions of extracorporeal shock wave lithotripsy were performed after ureteral stenting. Although disintegration and discharge of the stones were satisfactory, bladder stone induced by ureteral stent was complicated. The extracted bladder stone showed a yellowish brown color and the surface was granular shape. Composition of the stone was acetyl sulphapyridine which was a metabolite of salazosulphapyridine. After maintenance of the urinary pH ranges between 6.5 and 7.5 by medication of sodium bicarbonate, the patient remains free of stone for 3 years. Drug induced urolithiasis originated from salazosulphapyridine is extremely rare. Satisfactory oral fluid intake and urinary alkalization are important for prevention of sulpha drugs calculi of urinary tract.
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PMID:[A case of drug induced urolithiasis composed of acetyl sulphapyridine associated with ulcerative colitis]. 1034 5

A 56-year-old male with DM and HTN presented with flank pain and nausea. Review of systems was negative, physical examination was notable for mild hypovolemia and laboratory revealed BUN 51 mg/dl, creatinine (Cr) 5.1 mg/dl (baseline 1.5), Westergren ESR 122 mm/h, fractional excretion of sodium 0.2% and UA positive for blood and protein. Despite volume resuscitation the Cr continued to rise. Urine sediment analysis revealed granular casts, renal tubular epithelial cells and a negative Hansel's stain. Hemodialysis was initiated with Cr 13.7 mg/ dl for dyspnea and dysgeusia. Subsequent laboratory data revealed 2 separate positive anti-GBM antibody titers and prednisone therapy was initiated. Renal biopsy was performed for further diagnostic, therapeutic and prognostic information and demonstrated interstitial nephritis with linear IgG and albumin deposition consistent with diabetic nephropathy. Follow-up antibody titers were negative. prednisone was discontinued and Cr stabilized with conservative therapy. Anti-GBM antibody disease is characterized by circulating IgG antibodies directed against the glomerular basement membrane, specifically the alpha-3 (IV) collagen chain. Anti-GBM nephritis is a rapidly progressive, isolated glomerulonephritis in association with circulating anti-GBM antibodies. A positive immunofluorescence (IF) test is considered diagnostic in the appropriate clinical setting. Therapies include immunosuppressive agents to suppress new antibody production and plasmapheresis to eliminate circulating antibodies. Anti-GBM antibody is not rapidly cleared by steroid therapy and the recovery of renal function is rare if initiation Cr is greater than 7 mg/dl. This case demonstrates that the current ELISA for alpha-3 (IV) collagen is not pathognomonic for anti-GBM nephritis and that renal biopsy with IF for IgG and albumin may be indicated to prevent administration of potentially toxic treatment.
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PMID:Diabetic nephropathy with interstitial nephritis presenting with a false-positive anti-GBM antibody. 1203 99

We report a case of ammonium acid urate stone due to laxative abuse. A 27-year-old female complained of left flank pain. Computed tomography revealed bilateral ureter stones (right 16.5 x 9.0 mm; left 4 mm), while left ureter stone was radiolucent on the plain X ray film. Bilateral hydronephrosis was seen, but no therapy was performed for the right stone, because 99mTc-MAG3 scintigraphy revealed that right kidney had no function. The left stone was successfully removed by transurethral approach. The stone was revealed to be an ammonium acid urate by infrared spectrophotometry. She had been taking many laxatives (bisacodyl, sennoside, aloe extract) for 12 years to control her body weight. Ammonium acid urate stones are rarely seen in developed countries. We have reviewed 9 cases in Japan, describing ammonium acid urate stones due to laxative abuse. Among these patients, 24-hour urine volume and excretion in urinary sodium were decreased, and serum aldosterone was increased. The involvement of laxative abuse should be considered when ammonium acid urate is formed in a woman with a low body mass index.
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PMID:[Ammonium acid urate stone due to laxative abuse: a case report]. 1562 42

A 39-year-old Samoan man presented to the emergency department with fever, progressive weakness, and left flank pain of 1-month duration. For several months, he had also experienced progressive weight loss. There was no history of recent trauma, and he was not taking any medication. His medical history was notable for a large left groin abscess and left lower lobe pneumonia of unknown cause 1 year prior to the current admission. Furthermore, he had undergone exploratory laparotomy and gastric surgery for peptic ulcer disease approximately 10 years ago. Physical examination findings were positive for a tender firm mass in the left flank with no associated skin changes. Laboratory findings revealed an elevated white blood cell count of 18 x 10(9)/L. The urine cultures were negative. A computed tomographic (CT) image obtained 1 year prior to the current admission was unremarkable. CT of the abdomen and pelvis (section thickness, 5 mm) was performed after ingestion of 900 mL of 2% diatrizoate meglumine and diatrizoate sodium (Gastrografin; Bracco Diagnostics, Princeton, NJ). A 150-mL dose of iohexol (300 mg of iodine per milliliter) (Omnipaque; Nycomed, New York, NY) was administered intravenously at a rate of 4 mL/sec with a 70-second scan delay. Unenhanced CT images (not shown) did not reveal any areas of high attenuation.
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PMID:Case 117: actinomycosis of left kidney with sinus tracts. 1758 11


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