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

The clinical findings and sonographic observations in four patients with AFBN in childhood are described. AFBN in childhood is an acute interstitial nephritis presenting with septicaemia. The patients show a rapid deterioration of condition, weight loss, flank pain and often leucocyturia without detection of bacteria. The diagnosis is confirmed by renal sonography, showing typical focal alterations. Sonographic follow-up is important to prove the diagnosis. Even without detection of bacteria intravenous broad-spectrum antibiotic therapy is required. The antibiotic should be active against gram-negative organisms and Staphylococci. Medication should be given for 2-3 weeks. After adequate treatment the clinical condition will improve within a few days whereas sonographic alterations return to normal after 2-4 weeks. In childhood, a bacterial infection of other organs preceding AFBN is more common than anomalies of the urinary tract as predisposing factors. Therefore in most cases a hemotogenous infection must be presumed and its focus discovered and eliminated by appropriate antibiotics since otherwise AFBN may recur.
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PMID:[Acute focal bacterial nephritis in childhood]. 332 39

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

The diagnostic work-up of the urologic patient must be tailored to the presenting symptom complex, carefully selecting from the many modilities available, those most likely to establish the diagnosis and extent of the suspected lesions. Intravenous urography is the most rewarding initial procedure for many presenting symptoms, including suspected masses, pyuria, hematuria, and flank pain. Nuclear imaging is particularly effective in differentiating renal lobulations from true masses, in demonstrating parenchymal scarring in chronic pyelonephritis when the IVP is equivocal, and in assessing the decrease in perfusion and function in obstructive nephropathy when the IVP is indeterminate. It is the preferred procedure for acute renal infarction and acute tubular necrosis and has a greater sensitivity of detection for renal trauma than the IVP. Gallium-67 renal imaging appear helpful in the detection of occult pyelonephritis or interstitial nephritis. However, it cannot differentiate focal acute pyelonephritis from abscess or abscess from neoplasm. Ultrasoneography is the initial procedure of choice in the differentiation of cystic from solid renal masses and in anuria or oliguria. When a kidney fails to visualize by IVP or nuclear imaging, it can confirm or rule out obstruction. In upper tract infections, it may demonstrate renal or perirenal abscess. Although retrograde pyelography is performed less frequently in recent years, it remains extremely useful in confirming and relieving obstructive uropathy and in delineating tumors of the collecting system. Computed tomography effectively demonstrates hydronephrosis, renal abscess, tumors, and cysts and retroperitoneal involvement. More experience is needed to judge the efficiency of "dynamic" CT for the quantification of renal function. Renal angiography remains invaluable as a secondary procedure (as opposed to initial screening) in renal trauma, vascular anomalies, and in renal tumors to delineate the anatomy of the arterial supply and possible renal vein involvement.
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PMID:Medical imaging of renal diseases-suggested indication for different modalities. 724 59

High dosages of nephrotoxic drugs in elderly patients might be correlated with an increase in the number of patients with tubulo-interstitial nephritis (TIN). In patients with acute TIN, marked fever, back or flank pain, CVA tenderness, skin rash, arthralgia, eosinophilia, and eosinouria are observed. Clinical symptoms might be induced by glomerular, proximal tubular or distal tubular dysfunction in chronic TIN. Mild to moderate proteinuria, edema, hypertension, azotemia, glucosuria, aminoaciduria, polyuria and polydipsia are characteristic findings in patients with chronic TIN. These findings are slowly progressive in such patients. It appears that the marked fibrosis with lymphocyte infiltration in the interstitium is a poor clinical marker in patients with TIN. Furthermore, it is important to differentiate TIN from glomerulonephritis.
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PMID:[Symptoms in patients with tubulo-interstitial nephritis]. 756 29

A 48-year-old male experienced sudden pain in the right flank and macrohematuria with subsequent repeated episodes of painless macrohematuria. In the radiological work-up, CT was interpreted as inflammatory enlargement of the right kidney and MRI diagnosed renal vein thrombosis. There was some suspicion that there might be a malignancy. Five months later the patient had to be admitted to the hospital, because of increasing flank pain, desiccation and general signs of inflammatory disease. Radiological changes compatible with pulmonary metastases were found. Biopsy of enlarged mediastinal lymph nodes revealed undifferentiated carcinoma. Because of the expression of Cytokeratin primary urothelial carcinoma was suspected. The patient then deteriorated rapidly. No further specific therapy could be carried out. Death was chiefly caused by respiratory insufficiency 5 months after the first episode of pain and 1 month after admission. Autopsy revealed a poorly differentiated urothelial carcinoma of the right renal pelvis, with extensive carcinomatous angiomatosis and metastases to the left kidney, lungs, and regional and mediastinal lymph nodes. Independently of the carcinoma, both kidneys also showed interstitial nephritis, papillary necrosis and capillarosclerosis, compatible with analgesic-user kidney ("phenacetin kidney") in the absence of a corresponding history.
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PMID:[Explosive metastasis of a cancer of the kidney pelvis in analgesic kidney]. 815 79

Acute interstitial nephritis is a disease characterized by renal inflammation and is thought to be secondary to a hypersensitivity reaction. Although the causes of acute interstitial nephritis are numerous, adverse reactions to many common drugs, particularly antibiotics and nonsteroidal anti-inflammatory agents, are important etiological factors. Acute interstitial nephritis has many clinical manifestations, most notably fever and rash. Flank pain is an uncommon presentation. A case of acute, severe, low-back pain and rash in a healthy woman found to be secondary to acute interstitial nephritis is reported. The etiology of acute interstitial nephritis in this patient's case is suspected to be ranitidine (Zantac; Glaxo Pharmaceuticals, Research Triangle Park, NC), which has not been previously associated with this syndrome.
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PMID:Severe low back pain secondary to acute interstitial nephritis following administration of ranitidine. 828 78

We describe an unusual complication of acute pyelonephritis in a 45-year-old diabetic female. She was admitted to our hospital due to fever and flank pain which had developed 10 days earlier. Urinalysis showed many WBC and urine culture revealed Escherichia coli. After adequate antibiotic treatment, clinical symptoms abated but renal failure and leukocyturia persisted. Abdominal CT showed bilateral focal bacterial nephritis and renal biopsy disclosed chronic granulomatous interstitial nephritis. On the 80th hospital day she was discharged with a serum creatinine of 299 mumol/l. In the outpatient clinic, renal dysfunction and leukocyturia persisted up to 1 year. In conclusion, this case raises the possibility of a chronic interstitial process of acute pyelonephritis.
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PMID:Chronic granulomatous interstitial nephritis: unusual complication of acute pyelonephritis. 868 45

Cisplatin is a potent tubular toxin with a high incidence of nephrotoxicity. Carboplatin is considered less nephrotoxic but can still cause tubular injury and interstitial nephritis in patients who have been previously treated with cisplatin. The affected individuals usually have nonoliguric renal failure with a urine output of more than a liter per day. We present a 57-year-old white woman with no history of renal disease who underwent a total abdominal hysterectomy and bilateral salpingo-oophorectomy for stage IC ovarian carcinoma. One month later, she received chemotherapy with paclitaxel (Taxol) and carboplatin. On the following day, she developed frank hematuria and flank pain associated with a diminished urine output. Intravenous pyelogram (IVP) showed bilateral hydronephrosis with a total blockage of dye flow at the level of intraureteral lucencies consistent with bilateral blood clots. Her coagulation profile and uric acid was normal. Her acute renal failure (ARF) spontaneously resolved in the following 24 hours, with a brisk diuresis presumably due to clot lysis. The follow-up IVP showed a resolution of obstructive changes. A review of the literature shows a previous case in which high doses of carboplatin were implicated as the cause of hemorrhagic cystitis, presumably by toxicity to transitional epithelium of the bladder. We believe that the current case represents carboplatin-induced damage to the transitional epithelium in the renal pelvi and ureters causing gross hematuria and blood clots, resulting in bilateral ureteral obstruction and hydronephrosis.
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PMID:Carboplatin-related hematuria and acute renal failure. 1007 93

Indinavir sulfate has been reported to cause asymptomatic crystalluria and nephrolithiasis in patients with human immunodeficiency virus (HIV) infection. Patients taking indinavir may present with asymptomatic crystalluria, nephrolithiasis with frank renal colic and obstruction, flank pain in the absence of nephrolithiasis, and dysuria or urgency. Asymptomatic crystalluria has been described as benign. Discontinuation of the drug has not been recommended in the absence of nephrolithiasis. We report two HIV-positive patients receiving indinavir who developed acute interstitial nephritis with foreign body giant cell reaction on renal biopsies. Both patients had asymptomatic crystalluria, although crystals were associated with clumps of white blood cells (WBCs) on urinalysis in one patient. Both cases show that the inflammatory response was significant enough to lead to tubular injury and acute renal impairment. Our findings suggest that asymptomatic crystalluria attributable to indinavir may illicit an inflammatory response with acute renal insufficiency, warranting monitoring of renal function, especially in patients with crystalluria.
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PMID:Acute tubulointerstitial nephritis attributable to indinavir therapy. 1073 9


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