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

The pathophysiologic consequences of renal function impairment and chronic renal failure among others result from the loss of excretory and regulatory functions of the kidneys. The role of the exchange of cellular hydrogen ions of tubular fluid in the reabsorption of bicarbonate and in the urinary excretion of titratable acid and ammonia (acid-base regulation) is outlined. The effects of decreased glomerular filtration rate on calcium and phosphorus homeostasis are discussed. De novo urolithiasis in these patients is uncommon. However, it is well recognized that they may form matrix stones with calcium oxalate inclusions. Of greater significance is the prophylaxis in those patients, in whom urolithiasis has been the cause of chronic renal failure. In these patients it is of importance to modify the drug dosage or to abandon the prophylaxis when it interferes with the metabolic changes of renal function impairment. Some agents require no modification, others minor or major modifications. Some are even contraindicated. Hazards of stone prophylaxis in chronic renal failure: Acidification - cave metabolic acidosis! Cave RTA! Antibiotic agents - special rules to prevent accumulation. Thiazides - contraindicated! Hypokalemia; hyperuricemia; cave HPT! Triamterene - contraindicated! Acetazolamide (cystinuria) - contraindicated. Spironolactone - contraindicated. Sodium-cellulose-phosphate - Hyperoxaluria, hypomagnesiuria , hyperphosphatemia, cave HPT. Orthophosphate - cave urinary infection, cave poor renal function, cave obstruction. Allopurinol - dose reduction advisable. Brenzbromaron - contraindicated.
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PMID:[Prevention of calculus recurrence in impaired kidney function]. 653 25

The urinary excretion of calcium, oxalate, citrate and magnesium, and the relative saturation products in urine of either calcium oxalate or calcium phosphate, were determined in male duodenal ulcer (DU) patients preoperatively (n = 60), and 1 and 5 years following highly selective vagotomy (HSV), and in male healthy controls (n = 30). In DU before HSV citrate and magnesium were lowered, oxalate was in the low normal range and calcium was normal. The calcium oxalate product was lower than in controls, while the calcium phosphate product was unchanged. Within 5 years HSV normalized urinary citrate and oxalate, but not urinary magnesium, and the median urinary pH was lower than pre-operatively. There thus results a normal product for calcium oxalate, but a reduced one for calcium phosphate. It is suggested that: (1) unoperated DU patients have a urine composition similar to that exhibited in normocalciuric recurrent calcium urolithiasis; (2) this spectrum of urinary constituents may be changed by HSV.
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PMID:Urinary excretion of calcium, magnesium, oxalate and citrate in duodenal ulcer patients. Preliminary results before and up to five years after highly selective vagotomy. 663 26

Renal function evaluations were conducted on pullets and laying hens during outbreaks of urolithiasis. The following parameters were measured: kidney weights; hematocrits; plasma concentrations of uric acid, calcium, inorganic phosphate, magnesium, sodium, and potassium; urine flow rates; glomerular filtration rates; renal plasma flow rates; urine pH; and relative clearances of inorganic phosphate, calcium, magnesium, sodium, potassium, and para-amino hippuric acid. The adequacy of renal portal perfusion was estimated by timed phenol red extraction. Considerable interindividual variability was noted, presumably due to differences in age and reproductive status. Intraindividual left versus right kidney comparisons also were made, since urolithiasis often is associated with macroscopic lesions of one kidney but not the other. The results indicate that even when gross lesions of only one kidney were present, specific tubular transport processes were similar in both kidneys. Urolithiasis did cause significant alterations in urine flow rates, glomerular filtration rates and renal plasma flow rates. it was concluded that the changes associated with urolithiasis reflect the expected compensatory hypertrophic responses of surviving kidney tissue to a reduction of renal mass. The physiological impact of this form of kidney damage appears to arise from reduced renal mass rather than from inappropriate renal handling of minerals or electrolytes.
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PMID:Kidney function of pullets and laying hens during outbreaks of urolithiasis. 663 78

In order to study the mechanism of dystrophic calcification, an anoxic incubation of rat renal cortex in a tissue culture medium was performed in vitro. Calcium and phosphate in the medium were adjusted to 1.6 and 1.2 mM/1 respectively. Calcification occurred in apposition to the inner surface of membranous cellular degradation products and associated with the flocculent densities within the degenerate organelles. The chemical nature of the flocculent density was not determined. In view of the known affinity of calcium for acidic phospholipids, particularly phosphatidyl serine (PS), which lines the inner surface of the plasma membrane, calcification along the inner surface of membrane was thought to be related to the presence of PS. Accumulation of calcium in mitochondria, which is presumably dependent upon residual substrate for energy production, appeared to cause calcification as well. Amorphous calcium phosphate in the form of spheroids, and possibly fine fibrils and granules, also appeared to play a role in calcification by their transformation into apatite. The seemingly simple phenomenon of tissue calcification is complex. Nephrocalcinosis in vitro is remarkably similar to the calcification in acute tubular necrosis in vivo, and is a convenient model with which to study the mechanism of calcification. It is concluded that the cellular degradation products are the initial loci of calcification and have a likely role in urolithiasis.
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PMID:Nephrocalcinosis in vitro. 664 38

An outbreak of urolithiasis that doubled the annual mortality rate of chickens in a large flock of table-egg-layers is described. Despite the presence of a large unilateral urolith and/or severe renal atrophy, the layers often maintained active egg production and apparent homeostasis until a small urolith blocked the ureteral flow from the contralateral kidney. This terminal episode appeared to produce acute obstructive renal failure, rapidly developing visceral gout (visceral urate deposition), uremia, and death. The atrophy observed appeared to be acquired and progressive. Histologic features in the kidneys were acute to chronic glomerulonephritis, interstitial nephritis, and pyelonephritis. Epizootiologic and microbiologic studies indicated that a combination of infectious and noninfectious mechanisms may have been involved. Causative roles for calcium-phosphate imbalance, infectious bronchitis (IB), Newcastle disease (ND), and adenovirus or reovirus infections could be neither excluded nor confirmed. Contributory factors may have been spray ND-IB and other vaccinations of 15-week-old ND-IB-susceptible pullets, water deprivation, shipping stress, Mycoplasma synoviae infection, immune complex disease, and mycotoxins.
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PMID:Epizootiology, pathology, and microbiology of an outbreak of urolithiasis in chickens. 672 98

Over 97% of all uroliths in males less than a year of age and in females are phosphate, excluding males with portosystemic shunts and male Dalmatians . Uroliths in male Dalmatians usually are composed of urate. Uroliths associated with Staphylococcus aureus urinary tract infection are phosphate. About 60% of uroliths in adult male Basset Hounds , Bulldogs , Chihuahuas , Irish Terriers and Yorkshire Terriers are cystine. In males of other breeds, as high as 60% of uroliths are phosphate. Feeding a calculolytic diet (s/d: Hill's) results in phosphate urolith dissolution in 2-20 weeks. Long-term feeding of the calculolytic diet is not recommended, nor is use after surgery and in pregnant, lactating or growing dogs and in those with heart failure, edema, ascites or pleural effusions. Uroliths recur in 20-50% of affected dogs without subsequent dietary alteration. Use of a urolith-prevention diet (u/d: Hill's) is recommended if urolithiasis recurs.
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PMID:Canine urolithiasis: diagnosis and treatment. 673 11

Bone mineral content (BMC) was measured with the Norland Cameron apparatus in 120 renal stone formers (RSF) with idiopathic stone disease and in 41 patients with primary hyperparathyroidism. RSF were classified, according to an oral calcium load test, into three groups: no hypercalciuria (HC; 41 cases); absorptive HC (53 cases), and resorptive or renal HC (25 cases). BMC values in RSF as a group were significantly lower than normal (p less than 0.001, Mann-Whitney test) though higher than in hyperparathyroid patients. There was a trend for BMC to decrease from male RSF without HC to patients with renal or resorptive HC. No statistical difference was found between the groups, however, BMC values in absorptive HC were different from normal (p less than 0.001). Why patients with HC are demineralized is unclear since no correlation was found between BMC and basal values of serum phosphate, TRP, calculated TmP/GFR, urinary calcium or hydroxyproline. Nevertheless our results indicate that urolithiasis, and possibly its treatment, is not a benign condition for the skeleton.
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PMID:Bone mineral content in idiopathic renal stone disease and in primary hyperparathyroidism. 682 40

In a retrospective study of 120 patients with surgically proved primary hyperparathyroidism, 71 patients who were normotensive and 49 patients (41 percent) who were either hypertensive at the time of parathyroidectomy or had a history of hypertension were compared. The mean serum calcium levels in the normotensive and hypertensive patients were very similar (11.6 +/- 0.1 [SEM] mg/dl, and 11.8 +/- 0.1), ruling against the hypothesis that hypercalcemia per se is the dominant cause of the hypertension of hyperparathyroidism. The mean serum creatinine levels in the two groups were also very similar (1.02 +/- 0.05 and 1.09 +/- 0.05 mg/dl), indicating that the hypertension of hyperparathyroidism is not the consequence of advanced renal parenchymal damage. The hypertensive patients did not have a significantly higher prevalence of urolithiasis. A review of the data in this and related studies leads to the conclusion that the hypertension of hyperparathyroidism is heterogeneous in origin. The mean serum phosphate level in the hypertensive patients was significantly lower than that in the normotensive patients (2.20 +/- 0.06 mg/dl versus 2.69 +/- 0.09 mg/dl, p less than 0.02), which may be due to a decrease in renal tubular phosphate reabsorption secondary to hypertension.
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PMID:Hypertension and hyperparathyroidism. Inverse relation of serum phosphate level and blood pressure. 685 80

Crystal formation in whole urine was studied by the technique of rapid evaporation to 1,250 mosmol/l with and without raising citrate concentration by 40-50%. The added citrate reduced calcium oxalate crystal formation at pH 5.3 by about 25% and reduced calcium phosphate crystal formation at pH 6.8 by some 42%. These results support the view that citrate is important in maintaining calcium in solution in whole urine, and that raising the urinary citrate could be effective treatment for calcium oxalate/phosphate urolithiasis.
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PMID:Raising urinary citrate lowers calcium oxalate and calcium phosphate crystal formation in whole urine. 686 15

Hydroxamic acid, a potent urease inhibitor, having a high urinary excretion rate is expected to be a therapeutic agent for urolithiasis caused by urea-splitting bacterial infection of the urinary tract. Twenty-one new derivatives of N-aliphatic-acylglycinohydroxamic acids (GHAs) were synthesized, and their inhibitory potencies against the urease activity of sword bean in a phosphate buffer and against the ureolytic activity of Proteus mirabilis in human urine, and their urinary excretion rates in rats were also measured for this purpose I50 values of most of GHAs against the urease activity of sword bean were about 1 to 10 microM and 2-ethyl-n-butyroyl GHA was the most potent inhibitor with the value of 0.79 microM. I50 values of most of the GHAs against the ureolytic activity of Proteus mirabilis were about 5 to 50 microM and n-nonaroyl GHA was the most potent inhibitor with the value of 3.6 microM. 2,2-Dimethylpropionyl GHA had the highest urinary excretion rate with the recovery of 11%. Routes of administration of 2,2-dimethylpropionyl GHA and sex of rats used did not affect the amount of urinary excretion at all. The results in this report suggest that DL 2-methyl-n-butyroyl, 2-ethyl-n-butyroyl and 2,2-dimethylpropionyl GHA are the most hopeful therapeutic agents for urolithiasis among them.
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PMID:Therapy for urolithiasis by hydroxamic acids. III. Urease inhibitory potency and urinary excretion rate of N-acylglycinohydroxamic acids. 700 14


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