Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether extracorporeal shockwave lithotripsy (ESWL) for urolithiasis causes renal injury, we immunoassayed creatine kinase isozymes (CK-B and CK-M) in serum and urine from patients with renal stone (n = 21) and ureteral stone (n = 18) before and after (0, 2, and 24 h) ESWL. CK-B is generally present in renal tissue at relatively high concentrations, whereas CK-M is found at low concentrations. CK-B and CK-M levels were enhanced both in the serum and urine samples after ESWL in both groups of patients but CK-B levels return to almost normal very rapidly. Because CK-M, which is mainly localized in muscle tissue, also increased in both groups, the increased CK-B in serum after ESWL might be derived not only from kidney but also from muscle tissues which also contain a significant level of CK-B. These results suggest that significant tissue injury, including kidney and muscles, might be caused by ESWL treatment for urolithiasis but there is no long-term renal adverse effect, and that creatine kinase isozymes in serum and urine might be useful markers of tissue injury by such treatment.
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PMID:Effect of extracorporeal shockwave lithotripsy for urolithiasis on concentrations of creatine kinase isozymes in patient serum and urine. 141 5

In order to demonstrate that the extracorporeal shockwave lithotripsy (ESWL) for urolithiasis causes a renal damage, we immunoassayed S100a0 protein and creatine kinase isozymes (CK-B & CK-M) in the serum and urine from patients with renal stone (N = 21) and those with ureteral stone (N = 18) before and after ESWL. S100a0 protein and CK-B, which are localized in the proximal renal tubules at relatively high concentrations, were enhanced more or less both in the urine and serum samples after the treatment in both groups of patients. Since CK-M, which is mainly localized in muscle tissue, also increased in both groups of patients, S100a0 protein and CK-B may be derived not only from kidney, but also from muscle tissues.
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PMID:[S100a0 protein and creatine kinase isozymes (CK-B & CK-M) in serum and urine might be useful markers for non specific tissue damages by extracorporeal shockwave lithotripsy (ESWL)]. 192 Oct 18

Familial renal hypouricemia is a hereditary disease characterized by extraordinary high renal uric acid clearance and is associated with acute renal failure (ARF). An 18-year-old sumo wrestler developed ARF after anaerobic exercise. Several hours after the exercise, he had a pain in the loins with oliguria, headache, and nausea. On admission, his serum uric acid was decreased despite the elevation of serum creatinine (9.5 mg/dL). The level of creatine kinase was normal and there was no myoglobinuria or urolithiasis. Magnetic resonance imaging showed no significant abnormality. Renal function improved completely within 2 weeks of hydration treatment. After remission, hypouricemia became obvious (1.0 mg/dL) from the initial level of uric acid (6.1 mg/dL) and fractional excretion of uric acid was 49%. Polymerase chain reaction of a urate anion exchanger known to regulate blood urate level (SLC22A12 gene: URAT1) demonstrated that homozygous mutations in exon 4 (W258X). Both parents showed heterozygous mutation of the URAT1 gene, but both siblings showed no mutation. Thus, we describe a Japanese sumo wrestler of familial renal hypouricemia complicated with anaerobic exercise-induced ARF, with definite demonstration of genetic abnormality in the responsible gene, URAT1.
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PMID:Acute renal failure after exercise in a Japanese sumo wrestler with renal hypouricemia. 1909 27