Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0392525 (nephrolithiasis)
 2,669 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some neurophysiological techniques have been employed in clinical nephrology to record abnormalities of nervous conduction in central and peripheral pathways. The electrical monitoring on the peripheral and central nervous systems has allowed the detection of uremic neural injury, the diagnosis of specific electrophysiological abnormalities, the evaluation of various treatments employed and the identification of those abnormalities that uremia can induce. A group of 156 subjects subdivided into four groups were examined: 100 healthy subjects (64 M, 36 F); 56 patients (21 glomerulonephritis, 14 pyelonephritis, 5 nephrolithiasis, 5 polycystic kidney, 4 nephroangiosclerosis, 7 undetermined) with chronic renal failure treated with a conventional low nitrogen diet (CLND, 0.6 g/kg b.w./d. of proteins), 8 of whom passed from CLND to a very low nitrogen diet supplemented with alpha-keto-analogues; a group of 22 of these 56 underwent a regular dialysis treatment for 12 to 15 hours/weekly for 40.5 +/- 10.2 months. Three patients of the CLND group and 13 patients underwent renal transplantation after a variable period of RDT. In the uremic patients we found different populations of motor unit potentials; a decreased MNCV was found in 35% of the CLND patients, RDT patients had slowed MNCV in 42%. The SNCV was compromised more frequently than the MNCV. An increased duration of evoked potentials was sometimes observed in CLND and RDT patients inducing us to consider this a hallmark of uremic syndrome. The alpha-keto-analogues and HD/HP treated patients showed an improvement in several features.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrophysiological aspects of nervous conduction in uremia. 339 25

In humans, adenine phosphoribosyltransferase (APRT, EC 2.4.2.7) deficiency can manifest as nephrolithiasis, interstitial nephritis, and chronic renal failure. APRT catalyzes synthesis of AMP from adenine and 5-phosphoribosyl-1-pyrophosphate. In the absence of APRT, 2,8-dihydroxyadenine (DHA) is produced from adenine by xanthine dehydrogenase (XDH) and can precipitate in the renal interstitium, resulting in kidney disease. Treatment with allopurinol controls formation of DHA stones by inhibiting XDH activity. Kidney disease in APRT-deficient mice resembles that seen in humans. By age 12 wk, APRT-deficient male mice are, on average, mildly anemic and smaller than normal males. They have extensive renal interstitial damage (assessed by image analysis) and elevated blood urea nitrogen (BUN), and their creatinine clearance rates, which measure excretion of infused creatinine as an estimate of glomerular filtration rate (GFR), are about half that of wild-type males. APRT-deficient males treated with allopurinol in the drinking water had normal BUN and less extensive visible renal damage, but creatinine clearance remained low. Throughout their lifespans, homozygous null female mice manifested significantly less renal damage than homozygous null males of the same age. APRT-deficient females showed no significant impairment of GFR at age 12 wk. Consequences of APRT deficiency in male mice are more pronounced than in females, possibly due to differences in rates of adenine or DHA synthesis or to sex-determined responses of the kidneys.
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PMID:Chronic renal failure in a mouse model of human adenine phosphoribosyltransferase deficiency. 968 17

Calcium nephrolithiasis (CaNL) accounts for more than 70% of all renal stones, and its prevalence has increased in the last decades. Under this definition are included patients passing stones, composed of calcium oxalates and/or calcium phosphates. Current views of the pathogenesis of CaNL are based on the role of metabolic abnormalities which concur to render urines more conducive to crystallization. Therefore, the diagnostic approach is aimed at detecting these abnormalities, and the medical treatment assumes that a decrease in the risk of lithogenesis will result in remission or improvement of recurrences. The workup of the patients with CaNL begins with the analysis of passed stones and X-ray, sonography or other imaging techniques. Eligible patients, that is, both recurrent active stone formers and single-stone formers with individual risk factors, are considered for a metabolic evaluation, by which a number of blood and urine parameters are measured and others calculated. These include estimates of urine state of saturation with calcium and uric acid salts, net gastrointestinal alkali absorption, renal threshold of phosphate and other renal clearances and net acid and total nitrogen excretions. Basically, this screening is informative on renal function, metabolic abnormalities and their pathophysiology, risk of stone formation and dietary habits. During treatment it gives information about patient compliance and adverse effects of therapy. The cost of a comprehensive screening in Piedmont is 192,000 ITL (100 Euro) and rises to 300,000 ITL (154 Euro) if hormones and hydroxyproline are measured. In individual patients second- and third-level studies are performed, in order to detect systemic diseases which account for about 20% of CaNL in our series. Cost-to-benefit analysis has shown that the medical procedures for CaNL yield considerable saving in terms of difference between expenditure for drugs and testing and reduction of stone events. However, the current workup cannot be considered exhaustive, because misleading events may hamper the relation between laboratory findings and clinical outcome, and factors other than urine composition have appeared on the scenario of nephrolithiasis. These represent our challenge for the third millennium.
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PMID:Idiopathic calcium nephrolithiasis. 987 13

The purpose of this study was to determine the incidence of nephrolithiasis in radical cystectomy patients treated with either intestinal conduit or continent urinary diversion. The charts from 94 patients who had undergone radical cystectomy with urinary diversion at our institution from 1988 to 1998 were reviewed retrospectively for this study. Charts and radiographs from all patients were examined for renal function and evidence or urinary tract calculi. Two groups were compared: group I patients had undergone diversion with an intestinal conduit, and group II patients had received a continent diversion (primarily involving an Indiana pouch). Conduit diversions were typically done with a freely refluxing anastomosis (Bricker), whereas continent diversions were done with a nonrefluxing ureteral-intestinal anastomosis. Group I consisted of 54 patients who had undergone ileal conduit (50) or colon conduit (4) diversion with a mean follow-up of 2.5 years (range 0.6-7.0 years). Group II consisted of 40 patients who had undergone continent diversion (33 Indiana pouches, 7 orthotopic diversions) with a mean follow-up of 3.1 years (range 0.5-10.5 years). Laboratory studies of serum blood urea nitrogen, creatinine, and CO(2) were similar between the two groups. Six patients in group I developed urolithiasis, all in the upper tract. Stones developed at a mean of 3.1 years after urinary diversion. Three patients required operative intervention, whereas the others were managed expectantly. One patient in group II had an upper tract stone at the time of presentation for his bladder cancer, but no patient developed new upper tract stones during the present study period. Two patients in group II developed pouch calculi at a mean of 5 years after diversion; both required surgical intervention. In our study the risk for upper tract urolithiasis seemed higher in the intestinal conduit group (group I), with 11% of the patients developing stones. In the continent diversion group, no patient developed upper tract stones, although two patients (5%) developed pouch stones. Refluxing urine may contribute to an increased risk for stone formation after urinary diversion, whereas pouch stasis may contribute to stone formation in the continent diversion group.
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PMID:Incidence of urolithiasis in cystectomy patients after intestinal conduit or continent urinary diversion. 1055 49

The development of pharmacological counter-measures to the adverse effects of physiological adaptation to microgravity has received relatively more attention than alternatives such as dietary management. The manipulation of dietary cation-anion balance, and its subsequent effects on acid-base metabolism, have been routinely used for some time in managing domestic animal health. More recently, dietary intake by humans of alkalinizing potassium salts has been demonstrated to exert profound beneficial effects on calcium balance, bone mineralization, predisposition to calcium oxalate nephrolithiasis, and overall nitrogen balance. Dietary sodium restriction has also been shown to improve calcium balance, bone mineralization, and the effectiveness of neurohumoral defenses against orthostatic hypotension. It is proposed that these simple alterations in the astronauts' diets may be easily implemented to lessen the adverse effects of physiological adaptations to space flight, and to enhance or even replace prescribed pharmacological counter-measures.
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PMID:Dietary instead of pharmacological management to counter the adverse effects of physiological adaptations to space flight. 1120 Sep 75

Metabolic acidosis is an important acid-base disturbance in humans. It is characterised by a primary decrease in body bicarbonate stores and is known to induce multiple endocrine and metabolic alterations. Metabolic acidosis induces nitrogen wasting and, in humans, depresses protein metabolism. The acidosis-induced alterations in various endocrine systems include decreases in IGF-1 levels due to peripheral growth hormone insensitivity, a mild form of primary hypothyroidism and hyperglucocorticoidism. Metabolic acidosis induces a negative calcium balance (resorption from bone) with hypercalciuria and a propensity to develop kidney stones. Metabolic acidosis also results in hypophosphataemia due to renal phosphate wasting. Negative calcium balance and phosphate depletion combine to induce a metabolic bone disease that exhibits features of both osteoporosis and osteomalacia. In humans at least, 1,25-(OH)2 vitamin D levels increase, probably through phosphate depletion-induced stimulation of 1-alpha hydroxylase. The production rate of 1,25-(OH)2 vitamin D is thus stimulated, and parathyroid hormone decreases secondarily. There is experimental evidence to support the notion that even mild degrees of acidosis, such as that occurring by ingestion of a high animal protein diet, induces some of these metabolic and endocrine effects. The possible role of diet-induced acid loads in nephrolithiasis, age-related loss of lean body mass and osteoporosis is discussed.
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PMID:Metabolic and endocrine effects of metabolic acidosis in humans. 1141 68

The paper presents the results of operative treatment of complicated coral nephrolithiasis in 22 patients. Organ-saving operations were made in exacerbation of pyelonephritis with pyoseptic intoxication, severe renal failure with hyperazotemia. Partial nephrolithotomy (semisectional), sectional nephrolithotomy, resection of the kidney and coral calculus and calicolithotomy were made in 10, 1, 5 and 1 patients, respectively. As a rule, nephrolithotomy was completed with renal drainage by nephrostomy. After resection of a renal segment nephrostomy was not necessary. Postoperative complications did not occur. These occur only in 2 patients with bilateral coral calculi after nephrolithotomy and pyelolithotomy (urinary fistulas). To correct them, nephrostomy was made. One lethal outcome was caused by cardiovascular failure. The above surgery led to normalization of nitrogen-eliminating function of the operated kidney, elimination of intoxication and improvement of the patient's condition. Efficiency of the above operations recommends allows to recommend them for treatment of severe coral nephrolithiasis.
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PMID:[Surgical treatment of complicated forms of coral-like nephrolithiasis]. 1235 95

We reported that expression of both HSPG and of bikunin are increased in calcium oxalate (CaOx) nephrolithic rat kidneys (lida et al., J. Am. Soc. Nephrol. 1999, Urol. Res. 1997). However, these findings were obtained from separate experiments. The present study evaluates whether levels of HSPG and bikunin expression differ in the rat kidney during calcium oxalate nephrolithiasis. Twenty-four male Wistar rats weighing 200-250 g were assigned to one of four groups (n = 6 each group) and administered with 0.5% ethylene glycol daily and 0.5 microgram of 1 alpha-OH-D3 every other day to induce CaOx nephrolithiasis. Animals were sacrificed 1 or 2 weeks later and both kidneys were excised. The cortex was separated from the medulla and papillary tips in the right kidney, then stored in liquid nitrogen for quantitative competitive-reverse transcription-polymerase chain reaction (QC-RT-PCR). The left kidney was fixed in 10% buffered formalin for histochemical studies. We assessed the variable gene expression of both HSPG and bikunin by QC-RT-PCR. Immunohistochemical analyses of left kidney tissue samples determined the localization of HSPG and bikunin. Normal rats serving as controls (n = 6 each) were also sacrificed and processed in the same manner as the experimental groups. QC-RT-PCR confirmed that HSPG and bikunin mRNA expression is significantly increased in nephrolithic kidneys (p < 0.05; Mann-Whitney test), and that medulla and papillary tips tended to express more mRNA of both. Immunohistochemical studies revealed that the production of HS and bikunin was increased in both the distal and proximal tubules of nephrolithic kidneys. These findings suggest that the increased expression of both HSPG and bikunin play an important role during calcium oxalate stone formation. In addition, this phenomenon might be associated with the progression of urothelial damage.
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PMID:Heparan sulfate (HS)/heparan sulfate proteoglycan (HSPG) and bikunin are up-regulated during calcium oxalate nephrolithiasis in rat kidney. 1247 24

Humans although a predominantly ureotylic organism, has preserved the ability to excrete nitrogen as uric acid and ammonia. An imbalance between these two secondary modes of nitrogen excretion has resulted in uric acid precipitation in human urine. Uric acid nephrolithiasis can arise from diverse etiologies all with distinct underlying defects converging to one or more of three defects of hyperuricosuria, acidic urine pH, and low urinary volume, originating from secondary, genetic or heretofore undefined (idiopathic) causes. A subset of idiopathic uric acid nephrolithiasis (gouty diathesis) may be the "tip of the icebergp" of a broader systemic illness characterized by insulin resistance. A novel renal manifestation of insulin resistance is a mild defect in ammonium excretion, which is not severe enough to disturb acid-base homeostasis, but is sufficient to set up the chemical milieu for uric acid nephrolithiasis.
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PMID:Pathophysiology of uric acid nephrolithiasis. 1247 37

Melamine, a man-made non-nutritive substance containing nitrogen, can falsely elevate measures of protein content in foodstuffs. Several manufacturers of powdered infant formula in China apparently added melamine to raise the measured protein content and thereby exposed thousands of infants and young children to very high levels of melamine. Such exposure resulted in cases of acute kidney failure and nephrolithiasis. This Editorial from members of the world-wide Pediatric Nephrology community provides a common-sense approach to the care of infants who may have been exposed to powdered infant formula in 2007-2008.
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PMID:A position statement on kidney disease from powdered infant formula-based melamine exposure in Chinese infants. 1919 84


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