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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A retrospective study was conducted to characterize the diseases, clinical findings, and clinicopathologic and ultrasonographic findings associated with hypercalcemia (serum calcium concentration >11 mg/dL) in 71 cats presented to North Carolina State University Veterinary Teaching Hospital. The 3 most common diagnoses were neoplasia (n = 21), renal failure (n = 18), and urolithiasis (n = 11). Primary hyperparathyroidism was diagnosed in 4 cats. Lymphoma and squamous cell carcinoma were the most frequently diagnosed tumors. Calcium oxalate uroliths were diagnosed in 8 of 11 cats with urolithiasis. Cats with neoplasia had a higher serum calcium concentration (13.5 +/- 2.5 mg/dL) than cats with renal failure or urolithiasis and renal failure (11.5 +/- 0.4 mg/dL; P < .03). Serum phosphorus concentration was higher in cats with renal failure than in cats with neoplasia (P < .004). Despite the fact that the majority of cats with uroliths were azotemic, their serum urea nitrogen and creatinine concentrations and urine specific gravity differed from that of cats with renal failure. Additional studies are warranted to determine the underlying disease mechanism in the cats we identified with hypercalcemia and urolithiasis. We also identified a small number of cats with diseases that are not commonly reported with hypercalcemia. Further studies are needed to determine whether an association exists between these diseases and hypercalcemia, as well as to characterize the underlying pathophysiologic mechanism for each disease process.
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PMID:Hypercalcemia in cats: a retrospective study of 71 cases (1991-1997). 1077 91

Bacteria or their antigens persisting in the kidneys may induce the classical type of chronic pyelonephritis (CP), which progresses slowly, and may finally result in end-stage renal failure requiring dialysis. Pyelonephrogenic strains enter uro-epithelial and renal epithelial cells--where they accumulate--or may invade the renal interstitium. Promoting factors are obstruction, reflux, urolithiasis, nephrolithiasis, pregnancy, diabetes mellitus, humoral and cellular immunodeficiencies, immunosuppression treatment (e.g. following transplants), autoimmune phenomena (antigenic mimicry). Therapy comprises the treatment of underlying disease, antibiotics as indicated by the resistogram, acidification of urine (L-methionine), i.v. immunoglobulins (IgM, IgG) and oral vaccination with lyophilized uropathogens.
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PMID:[Chronic pyelonephritis. Synopsis of laboratory values and ultrasound lead to diagnosis]. 1090 12

Unexplained hypercalcemia has been increasingly recognized in cats since 1990. In some instances, hypercalcemia has been associated with calcium oxalate urolithiasis, and some affected cats have been fed acidifying diets. We studied the laboratory findings, clinical course, and treatment of 20 cats with idiopathic hypercalcemia. Eight (40%) of the cats were longhaired and all 14 cats for which adequate dietary history was available had been fed acidifying diets. Clinical signs included vomiting (6 cats), weight loss (4 cats), dysuria (4 cats), anorexia (3 cats), and inappropriate urinations (3 cats). Hypercalcemia was mild to moderate in severity. and serum parathyroid hormone concentrations were normal or low. Serum concentrations of phosphorus, parathyroid hormone-related peptide, 25-hydroxycholecalciferol, and calcitriol were within the reference range in most cats. Diseases commonly associated with hypercalcemia (eg, neoplasia, primary hyperparathyroidism) were not identified despite thorough medical evaluations and long-term clinical follow-up. Azotemia either did not develop (10 cats) or developed after the onset of hypercalcemia (3 cats), suggesting that renal failure was not the cause of hypercalcemia in affected cats. Seven of 20 cats (35%) had urolithiasis, and in 2 cats uroliths were composed of calcium oxalate. Subtotal parathyroidectomy in 2 cats and dietary modification in 11 cats did not result in resolution of hypercalcemia. Treatment with prednisone resulted in complete resolution of hypercalcemia in 4 cats.
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PMID:Idiopathic hypercalcemia in cats. 1111 Mar 84

Evaluation of the risk for developing renal insufficiency is generally not considered during the clinical metabolic workup of the stone-forming patient. This review approaches the problem of the severity of nephrolithiasis by addressing the renal risk. Although renal stones are an infrequent cause of renal failure, some lithiasic forms present a greater risk, such as in hereditary stone diseases (eg, cystinuria, primary hyperoxaluria, Dent's disease), primary struvite stones, and infection-related urolithiasis associated with anatomic and functional urinary tract anomalies and spinal cord injury. Recurrent bouts of obstruction and/or crystal-specific biological effects on tubular epithelial cells and interstitial renal cells may activate the fibrogenic cascade responsible for the loss of renal parenchyma. In clinical terms, frequent stone relapses, episodes of urinary tract infection and obstruction, number of urological interventions, and size of the gravel are all significantly associated with the risk for renal failure. Percutaneous and extracorporeal urological methods for the treatment of renal stones may also lead to some chronic deterioration of renal function, particularly in recurrent stone formers treated with multiple therapeutic sessions. Although still speculative, concerns exist about the effect of extracorporeal shock wave lithotripsy on small or pathological kidneys. Without doubt, the medical prevention of stones would be more sensible.
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PMID:Risk for renal failure in nephrolithiasis. 1115 64

163 patients with urolithiasis of the solitary kidney were treated surgically. Analysis of causes of postoperative complications (n = 70) and lethal outcomes (n = 11) demonstrate that lethal outcomes were in many cases related to exacerbation of renal failure, acute calculous pyelonephritis which had provoked sepsis and bacteriotoxic shock, acute hemorrhage with hemorrhagic shock followed by development of DIC-syndrome.
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PMID:[Risks and complications of surgical treatment of urinary lithiasis of single kidney]. 1156 32

Hypoxanthine-guanine phosphoribosyltransferase (HPRT) deficiency is an X-linked defect of purine metabolism. Clinical manifestations are usually related to the degree of enzyme deficiency: complete HPRT deficiency (Lesch-Nyhan syndrome) presenting with severe neurologic or renal symptoms, or partial HPRT deficiency (Kelley-Seegmiller syndrome) manifesting as a gout-urolithiasis syndrome. A 3-generation kindred is described in which the recognition of partial HPRT deficiency in 2 adolescent male siblings presenting with uric acid lithiasis led to the diagnosis in 2 maternal uncles already in renal failure of unknown cause. This report highlights the importance of clinical awareness leading to early diagnosis, appropriate diagnostic methodology, and therapy of a treatable inherited disorder of purine metabolism for the prevention of renal failure.
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PMID:Partial hypoxanthine-Guanine phosphoribosyltransferase deficiency as the unsuspected cause of renal disease spanning three generations: a cautionary tale. 1177 85

Primary hyperoxaluria type 1 (PH1) is an inherited metabolic disorder characterized by recurrent urolithiasis and nephrocalcinosis frequently leading to progressive renal insufficiency during the second decade of life. Systemic organ involvement as a result of the accumulation of calcium oxalate crystal deposits in vessel walls often is observed. We report a case of a 56-year-old woman with late-onset of PH1 who developed rapidly progressive renal failure and severe systemic oxalosis with skin and eye involvement despite intensified hemodialytic therapy during the waiting period for combined liver and kidney transplantation. This case illustrates the difficulties in treatment of PH1-induced end-stage renal disease. Combined liver and kidney transplantation should be offered to these patients as soon as possible to reverse the underlying metabolic defect and to restore renal function.
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PMID:A case of late-onset primary hyperoxaluria type 1. 1184 Apr 2

236 operative interventions for urolithiasis have been performed in 234 patients. Of them, 187 (79.9%) patients developed complications. Intraoperatively complications resulted from opening of the pleural and abdominal cavities (20 patients, 8.5%) and intraoperative blood loss < 500 ml (19 patients, 8.1%). In one case a nephrectomy was made because of repeated hemorrhage early after the operation. Among the postoperative complications most frequent were acute pyelonephritis (34, 14.5%) and aggravation of renal failure (11, 4.7%). The former demanded extracorporeal detoxication in 9 cases, in the latter hemodialysis was not required. Residual comcrements occurred in 28 (12%) patients. 17 of them had to undergo extracorporeal lithotripsy. Thus, open urological interventions in urolithiasis are now conducted in advanced disease, provoking complications. This raises responsibility of the surgeons who must take maximal preventive measures and use novel technologies in management of the complications.
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PMID:[Complications of open surgical procedures in urolithiasis and their prevention]. 1257 69

Primary hyperoxaluria type 1 (PH1) usually presents with recurrent urolithiasis, nephrocalcinosis and progressive renal failure at a relatively young age. This report describes a patient who, due to the late onset of end-stage renal disease, had been diagnosed with PH1 only after failure of his second kidney graft. Retrospectively, his vascular problems, skeletal abnormalities and cardiac arrhythmias fit the picture of severe systemic oxalosis. Possible therapeutic options are discussed.
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PMID:Renal graft failure due to type 1 primary hyperoxaluria. 1260 92

Cystinuria is an autosomal recessive defect in transepithelial transport of dibasic amino acids (e.g. cystine) which involves the proximal canaliculi, small intestine and central nervous system. It is the least common cause of nephrolithiasis, accounting for 1 to 3% of renal calculi. The natural course of the disease, characterised by recurrent stone formation, can frequently lead to renal failure, if left untreated. Until recently, treatment of cystinuria has been limited to symptomatic management including intensive hydration and urine alkalinisation. Different drugs that react with cystine to form soluble complexes have been used but their efficacy remains questionable. We present the case of a 6-year-old boy with severe, recurrent cystine urolithiasis treated with captopril. The diagnosis of cystine urolithiasis was established after a 3-year course of clinically apparent nephrolithiasis, characterised by stone passage. At the age of 5 years he underwent lithotripsy and nephrolithotomy for removal of staghorn calculi. Since then treatment with citrate and magnesium supplementation combined with captopril was introduced. After a follow-up of 12 months the patient remained stone-free. Urinary cystine decreased from 230 to 136 mg per gram creatinine. We conclude that captopril can be useful in the treatment of cystine urolithiasis in children.
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PMID:[Beneficial effect of angiotensin converting enzyme inhibitor treatment in severe cystine urolithiasis]. 1291 8


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