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PubMedDate not supplied

[Dent's disease: hereditary nephrolithiasis related to defective tubular endocytosis processes].

Dent's disease, a X-linked hypercalciuric nephrolithiasis, is caused by mutations of the CLCN5 gene. The disease is characterised by low molecular weight proteinuria with variable presence of hypercalciuria, hyperphosphaturia, nephrocalcinosis, and kidney stones. CLCN5 encodes a chloride channel belonging to the voltage-gated chloride channel family, which is predominantly expressed in the endosomes of proximal tubular cells. By shunting the current of electrogenic H+-ATPase, ClC-5 is crucial for efficient acidification of renal endosomes. As shown in knock-out mouse models, the ClC-5 loss of function causes severe impairment of receptor-mediated endocytosis, as well as the endocytotic retrieval of plasma membrane proteins including megalin. In a minority of patients with classical Dent's disease, the analysis of CLCN5 coding sequences failed to identify causative mutations. It is conceivable that mutations in the 5' upstream regulatory regions could impair the correct processing and translation of CLCN5. The complexity of its promoter region seems to support this hypothesis. Molecular diagnosis of Dent's disease is now available; since the risk of developing renal insufficiency in adult life is elevated for this type of nephrolithiasis, the correct diagnosis could potentially modify the natural history of the disease by preventing the evolution towards uraemia.

Animals↗

PubMedDate not supplied

Laparoscopic pyeloplasty and flexible nephroscopy: simultaneous treatment of ureteropelvic junction obstruction and nephrolithiasis.

BACKGROUND AND OBJECTIVE: Ureteropelvic junction obstruction and concomitant calculus disease may coexist. Therapeutic controversy exists regarding their ideal management. We report our use of flexible nephroscopy during laparoscopic pyeloplasty for caliceal stone removal. METHODS: From August 1998 through May 2002, 50 laparoscopic pyeloplasties were performed. Seven patients had documented ureteropelvic junction obstruction and ipsilateral nephrolithiasis. Preoperative stone burden and location were assessed. After pyelotomy, a 16 Fr flexible endoscope was passed through the uppermost trocar under direct laparoscopic guidance into the collecting system. Stone extraction was performed with a 2.4 Fr Nitinol basket. Postoperative imaging was assessed. RESULTS: Complete stone-free status confirmed by postoperative imaging was achieved in 6 of 7 patients. The longest individual stone diameter ranged from 4 mm to 13 mm (mean, 10.3 mm), and an average of 2.5 stones per patient was removed (range, 1 to 4 stones). Neither intraoperative fluoroscopy nor lithotripsy was required. No intraoperative or delayed complications were noted during a mean follow-up of 8.5 months (range, 2 to 17 months). CONCLUSIONS: Laparoscopic pyeloplasty and concomitant flexible nephroscopy with basket extraction is a simple, attractive alternative for the simultaneous treatment of ureteropelvic junction obstruction presenting with coexisting nephrolithiasis. It appears more efficacious when the stone number is limited and diameters measure from 5 mm to 20 mm.

Adult↗

PubMed2004

Dent's disease--a nephrolithiasis disorder associated with defective receptor-mediated endocytosis.

Dent's disease, a renal tubular disorder characterized by low-molecular-weight proteinuria (LMWP), hypercalciuria, and nephrolithiasis, is due to inactivating mutations in the x-linked renal specific chloride channel CLC-5. CLC-5 belongs to the family of voltage-gated chloride channels, which function as homodimeric proteins with each subunit consisting of 18 helices and a chloride selectivity filter, i.e. pore. None of the 15 CLC-5 missense mutations reported in patients with dent's disease involves the chloride selectivity filter, but 12 of these are clustered around the interface of the two subunits, thereby emphasising the important role for the interaction between the two subunits at the interface of the homodimeric CLC-5. In the kidney, CLC-5 forms part of the receptor-mediated endocytic pathway, and defects in this pathway due to a loss of CLC-5 function, may help to account for the LMWP, hyperphosphaturia, hypercalciuria and nephrolithiasis. The molecular studies and the generation of mouse models of the disease have increased our understanding of the renal tubular mechanisms that regulate mineral homeostasis.

Calcium↗

PubMedDate not supplied

Prevalence of fasting hypercalciuria associated with increased citraturia in the ambulatory evaluation of nephrolithiasis.

BACKGROUND: Nephrolithiasis is a common, high costing pathology of the urinary tract. The most common urinary abnormalities are fasting hypercalciuria, hypercalciuria and hypocitraturia. This study aimed to identify the principal urinary abnormalities in our patients. METHODS: Ninety-eight patients (pts) (43 females, 55 males) with recurrent calcium nephrolithiasis underwent metabolic evaluation. In two 24-hr urine collections the following parameters were evaluated: calcium, phosphate, sodium, potassium, chloride, magnesium, citrate, oxalate, uric acid, creatinine (Cr), urea, ammonium and pH; blood measurement of calcium, phosphate, sodium, potassium, chloride, magnesium, uric acid, Cr, urea, acid-base balance ionized calcium and intact parathyroid hormone (iPTH) were also performed. A first morning voided urine sample was collected for measuring the urinary cross-links and fasting calciuria. The tubular threshold of phosphate (TmP) was calculated according to Walton and Bijovet. Metabolic evaluation was repeated in 63/98 pts after 7 days on a low calcium diet. RESULTS: The most common urinary abnormalities were fasting hypercalciuria in 51/96 pts (53.1%), hypercalciuria in 33/97 pts (34%) and hypocitraturia in 29/98 pts (29%); 24/33 pts (73%) with hypercalciuria had fasting hypercalciuria. Hypercalciuria was partially corrected on the calcium-restricted diet, while fasting hypercalciuria was not. Urine citrate levels were significantly higher in patients with fasting hypercalciuria. CONCLUSIONS: Fasting hypercalciuria was the most frequent urinary abnormality and it was not corrected with a calcium-restricted diet. In fasting hypercalciuric patients, increased bone resorption activity could be responsible for higher citraturia levels.

Calcium↗

PubMed1992

Idiopathic calcium oxalate nephrolithiasis: a cellular disease.

Physico-chemical, metabolic and hormonal theories regarding the pathogenesis of calcium oxalate nephrolithiasis do not sufficiently explain many features of this disease. The recent findings of an abnormally faster oxalate self-exchange and higher phosphorylation of band 3 in erythrocytes of idiopathic calcium oxalate stone formers suggest the hypothesis that nephrolithiasis may be a cellular disease, characterized by a defect in the function of the anion-exchange. The cellular anomaly seems genetically controlled. Band 3 anion exchanger function seems to be biochemically regulated through modulation of band 3 phosphorylation, which depends on cyclic AMP- and phospholipid-sensitive Ca2+ independent protein kinases. In this light, a reduced glycosaminoglycan concentration in the erythrocyte membranes of stone formers might play a role, as these molecules exert a strong inhibitory effects on band 3 phosphorylation and anion transport in vitro and in vivo. An in vivo trial was performed in which stone formers were administered glycosaminoglycans orally. A reduction in oxalate excretion, and oxalate renal clearance, and a simultaneous correction of the abnormal RBC oxalate flux and band 3 phosphorylation were observed. These data suggest the existence of a link between the erythrocyte abnormality and oxalate transport by the kidney and gut.

Animals↗

PubMed1991

Renal excretion of citrate in patients with chronic renal failure or nephrolithiasis.

Using a specific citrate lyase method, renal excretion of citrate was studied in 32 normal Chinese males, 30 nondialysed uremic male patients and 35 male subjects who had a history of nephrolithiasis. Patients with uremia or nephrolithiasis were found to have a lower urinary citrate excretion. Tubular reabsorption of citrate was markedly decreased in uremic patients, but in stone patients, the increased renal tubular reabsorption of citrate was only found in patients with hypocitraturia, whose renal citrate excretion was below 650 mumol/day and whose urinary magnesium was also low. Hypocitraturia was found in 45% (16/35) of the patients with renal stones whether their filtered load of citrate was normal or subnormal. Urinary citrate excretion was correlated with renal creatinine clearance in both normal subjects and in patients with renal stones or chronic renal failure. However, urinary phosphate correlating with urinary citrate was only found in normal subjects and in patients with kidney stones. In normal subjects, we found a positive correlation between urinary citrate and phosphate, but in stone patients, we found a negative correlation. Hypercalciuria and hyperoxalaturia were noted in some stone formers, who had, moreover, a lower urinary citrate and ascorbate excretion level. Mean urinary ascorbate excretion in patients with renal stones was markedly below that in normal subjects. Thus, we suggest that low urinary citrate excretion may be prevalent in patients with renal stones or chronic renal failure, and that hypocitraturia can be found in some stone formers, whose tubular reabsorption of citrate may be increased.

Adult↗

PubMedDate not supplied

[The comprehensive examination of patients with recurrent calcium nephrolithiasis].

Hypercalciuria is one of the main causes of recurrent generation of urinary calcium-containing calculi. 107 patients with recurrent calcium nephrolithiasis were examined and results presented. Concentrations of potassium, sodium, chlorides, calcium, phosphorus, uric acid and creatinine were investigated in serum and urine, as well as indices of acid-base balance in arterial blood. pH-metry, "preliminary" and oral calcium tolerance test were also carried out. The microcomputer data analysis established that the diagnosis of primary hyperparathyroidism may be identified in case of increased serum calcium level before and after calcium load test, the same of parathyroid, and increased urinary cAMP excretion. Renal hypercalciuria is characterized by low blood calcium level in both periods of the oral test, high basal calciuria, increased urinary cAMP excretion and its slight decrease after the oral calcium load test, by a tendency to lower serum magnesium levels in high magnesuria. The patients with absorptive hypercalciuria had an upper normal or increased blood calcium level, a significant calcemic and calciuric "response" to the calcium load, reduction in urinary cAMP elimination and more severe decrease (close to 0) of these indices after oral calcium load and normal magnesium levels in blood and urine. On a base of the "preliminary" test data the patients with relapsing calcium nephrolithiasis and metabolic disorders may be differed from those without calcium and phosphorus metabolic deteriorations. The "preliminary" test defines indications for the oral calcium tolerance test, automatic diagnosis and computer data storage facilitate physician to work and to solve problems of the patients' survey.

Calcium↗

PubMedDate not supplied

[The nature of the homeostatic changes in nephrolithiasis patients].

Rheorenographic findings, activities of 4 major glycolytic enzymes and 3 Krebs cycle ones in serum and blood, urinary fibrinolytic activity were analyzed in 117 patients with coral nephrolithiasis (the pelvis was drained after calculus removal) in 114 patients with non-coral calculi (the pelvis was sutured) before and 7, 14 days after surgery. Rheography revealed a significant decrease in arterial vascular tone and blood filling and an impairment in venous return in the diseased kidney. In the patients with nephrolithiasis, the enzymatic activity showed 3.5-10.5- and 4.5-11.5-fold increase (p less than 0.001) in the Krebs cycle and glycolysis, respectively, suggesting activation of not only oxidative phosphorylation, but anaerobic glycolysis. Tubular metabolic acidosis occurred, which made the enzymes enter blood and urine from the epithelial cells. On days 7-14 of postoperation, rheographic parameters, enzymatic and fibrinolytic activities of the urine remained virtually unchanged as compared to the values observed in the preoperative period. Moreover, the patients with a sutured pelvis showed highly accelerated glycolysis during the surgery against prior to the procedure. Urinary mitochondrial enzyme release increased, which reflected an enhancement of degenerative changes in nephron cells. Urinary fibrinolytic activity remained lower. In the patients with a drained pelvis, all the parameters in question became better.

Adult↗

PubMed1991

[Oxalate influx rate in red blood cells in calcium oxalate nephrolithiasis].

We established a method of human red blood cell oxalate influx rate under the condition of steady state exchange. Using this method we measured the influx rate in 10 patients with recurrent calcium oxalate nephrolithiasis and in 18 controls. DIDS inhibited oxalate flux across the human red blood cell membrane. This result suggested that band 3 protein mediates oxalate transport. Oxalate influx rate depended on reaction temperature and pH of reaction buffer. Although the oxalate influx rate in 4 degrees C could not be determined under an initial condition rate, the measurable condition was in 0 degrees C of reaction temperature. Consequently we measured the oxalate influx rate under the condition of 0 degrees C reaction temperature and 20 ml volume of washing buffer. The mean oxalate influx rate was significantly higher in patients with nephrolithiasis than in controls (-1.00 +/- 0.19 vs. -0.78 +/- 0.14).

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1990

The role of diet in the pathogenesis and therapy of nephrolithiasis.

The epidemic of nephrolithiasis in the developed world in the twentieth century is in part the result of the diet consumed in these affluent nations. High protein intake is probably the most important factor. The patients who develop nephrolithiasis may have an increased calciuric response to diet protein and perhaps to diet sodium. The benefits of dietary modification include not only a tendency to reduce urinary calcium excretion but also increased urinary citrate and reduced urinary oxalate excretion. High fluid intake is also an important component of the therapeutic armamentarium of the physician treating patients with recurrent stone formation. The benefit of dietary therapy in patients with recurrent stone formation has not as yet been rigorously tested in controlled studies. Furthermore, there are few valid clinical studies of various pharmacologic agents such as thiazides, phosphates, allopurinol, and citrate. In the absence of clear-cut advantage of any specific pharmacologic agent, it appears that many patients may benefit from dietary modification rather than embarking on a life-long use of medications to prevent stone recurrences.

Calcium↗

PubMed1990

Obstructive nephrolithiasis and ureterolithiasis associated with chronic renal failure in horses: eight cases (1981-1987).

Eight adult horses with obstructive nephrolithiasis and/or ureterolithiasis were examined between 1981 and 1987. One horse had bilateral ureteral obstruction at hospital admission; the others had unilateral ureteral obstruction. All horses had similar bilateral renal pathologic findings that were compatible with chronic intermittent or complete obstruction. Horses were referred for evaluation of weight loss, poor performance, and/or decreased appetite. Clinical findings, laboratory results, and/or postmortem findings in all horses supported the diagnosis of chronic renal failure. Age of the 8 horses varied between 2 and 17 years; 5 of the 8 were between 2 and 3 years old. Seven horses were Thoroughbreds and 1 was a Standardbred. Of the horses examined, 4 were females and 4 were males (2 geldings). Diagnosis of obstructive nephrolithiasis and/or ureterolithiasis was made in all of the hospitalized horses based on examination per rectum and/or renal ultrasonographic findings. Surgical removal of the obstructing calculi was performed in one horse. Although etiopathogenesis could not be proven, histopathologic findings in the kidneys of the horses of our study were suggestive of renal failure secondary to obstructive urinary disease.

Animals↗

PubMedDate not supplied

[Primary hyperparathyroidism in patients with bilateral nephrolithiasis].

Experience in the diagnosis and treatment of the renal form of primary hyperparathyroidism in 57 patients with bilateral nephrolithiasis was summed up. The main diagnostic criterion was the detection of biochemical changes in the blood and urine (hypercalcemia, hypophosphatemia, hypercalciuria) and the use of some tests (Howard's test and parathyroidin test). Parathyroidectomy was performed after establishing diagnosis. A new stage in therapy of such patients was a study of renal function and phosphocalcium metabolism after parathyroidectomy. The improvement of some indices (an increase in glomerular filtration, urea excretion with urine and relative urine density, and a decrease in hypercalciuria and hyperphosphaturia) indicated the effectiveness of surgical intervention for primary hyperparathyroidism in patients with bilateral nephrolithiasis. It was also confirmed by a decrease in lithogenic relapse after parathyroidectomy.

Arteries↗

PubMed1989

Nephrolithiasis in pregnancy.

Nephrolithiasis is a rare but important condition in pregnant women. The most common presenting complaint is flank pain. Recurrent or persistent urinary tract infections may also be due to nephrolithiasis. Ultrasound is the first-line diagnostic study, but a limited intravenous pyelogram can be obtained when indicated. Spontaneous passage of the stone occurs in approximately two-thirds of patients.

Female↗

PubMed1989

[New pathophysiologic aspects of nephrolithiasis].

Urinary supersaturation with stone-forming ions is the driving force of crystallization in renal tubules. Based on concentration measurements of the majority of ions, supersaturation can be calculated by means of a computer program. Assessments of 24-hour urine excretions of lithogenic substances do not necessarily detect intermittent supersaturation which may induce crystallization processes. Even the most elaborate metabolic evaluations fail to detect metabolic abnormalities in 10-30% of unselected patients with nephrolithiasis ("idiopathic" nephrolithiasis). Apart from supersaturation, crystal aggregation seems to be a most important factor in kidney stone formation whose pathophysiologic relevance has so far been underestimated. New studies demonstrate excellent inhibition of calcium oxalate monohydrate crystal aggregation by nephrocalcin and Tamm-Horsfall glycoprotein, 2 glycoproteins produced by the kidneys. In recurrent "idiopathic" calcium oxalate stone formers both proteins are structurally and functionally defective crystal aggregation inhibitors.

Calcium Oxalate↗

PubMed1987

Renal tubular dysfunctions in patients with idiopathic calcium nephrolithiasis.

To define the degree of renal tubular involvement in idiopathic calcium nephrolithiasis, 18 patients (aged 23-60 years, 15 men and 3 women, with 1-30 years of renal stone history) with normal glomerular filtration rate (GFR) and effective renal plasma flow with no history of urinary tract infection and on no dietary or drug therapy underwent the following studies: measurement of proximal tubular maximum reabsorption of glucose (Tmglucose) and secretion of para-aminohippurate (TmPAH), urinary concentrating ability after 14 h of fluid deprivation, and urinary net acid excretion following an oral dose of ammonium chloride, 0.1 g/kg of body weight. Seventeen healthy subjects in the same age range served as control. Patients with calcium nephrolithiasis, with normal renal hemodynamic functions, have significantly lower proximal tubular maximum reabsorptive and secretory functions, diminished urinary concentrating mechanism, and reduced urinary net acid excretion following an oral acid load. These tubular functional abnormalities were observed in patients with or without hypercalciuria.

Adult↗

PubMed1979

Idiopathic calcium nephrolithiasis. 1. Differences in urine crystalloids, urine saturation with brushite and urine inhibitors of calcification between persons with and persons without recurrent kidney stone formation.

The propensity of urine to promote calcium stone formation was compared in 64 patients with recurrent idiopathic calcium nephrolithiasis and 30 healthy individuals without such a history. The rates of excretion of urine crystalloids, the urine saturation with brushite (CaHPO4-2H2O), the ability of the urine to calcify collagen in vitro, and the concentration of urine inhibitors of collagen calcification were measured. The patients had a reduced urine citrate excretion rate in addition to an increased urine calcium excretion rate, while the rates for urine magnesium, phosphate, uric acid and oxalate were not significantly different in the two groups of subjects. The urine concentration of magnesium, phosphate and uric acid was decreased in the patients because of the higher urine volume. The urine creatinine excretion rate correlated with the rates of excretion of urine calcium, magnesium, phosphate, uric acid and oxalate in both groups, which suggested that increased lean body mass, possibly associated with greater food intake, may be an important determinant of crystalloid excretion. The urine of the patients was significantly more saturated with brushite than the urine of the control subjects and resulted in greater collagen calcification when incubated in vitro. The urine concentration of inhibitors of collagen calcification, however, was not significantly different in the two groups. Thus, the urine of patients with recurrent idiopathic calcium nephrolithiasis is more highly saturated with brushite, largely as a result of an increased urine calcium excretion rate, and contains a lower concentration of magnesium and citrate, substances that tend to prevent the precipitation and growth of crystals in urine.

Adult↗

PubMed1979

[Recent advances in the treatment of nephrolithiasis (author's transl)].

The treatment of nephrolithiasis depends mainly on the type of stone present. Uric acid calculi can be dissolved by oral medication producing alkalinization of the urine. Cystin stones can only rarely be dissolved by oral administration of D-penicillamine. The best and least expensive prophylaxis is a high and constant fluid intake of 600 ml every 4 hours. This way the pathologically increased cystin excretion can be kept soluble. Calcium containing calculi and so-called "infection stones" need surgical intervention. Because of the high recurrence rate of renal stones every indication for an operative procedure has to be considered very carefully. For lasting results elimination of urinary obstruction is necessary. The treatment of choice of patients with staghorn calculus disease is surgical, even in the solitary kidney and in geriatric patients. As recent advances in the operative treatment of nephrolithiasis coagulum pyelolithotomy, intraoperative pyeloscopy, hypothermia and "bench surgery" (extra-corporeal renal surgery) are reviewed. Attempts to dissolve renal calculi by percutaneous nephrostomy as well as extraction of pelvic stones by the same procedure are mentioned. Finally, the importance of postoperative prophylaxis and the progress made in the medical treatment of calcium stones are pointed out.

Calcium↗

PubMedDate not supplied

[Calcium nephrolithiasis and phosphate therapy. Long term study (65 cases) (author's transl)].

Protected phosphate therapy was used in 65 cases of recurrent calcium nephrolithiasis. Mean duration treatment was 2 years and 1 month (more than 3 years in 17 cases). Mean lithiasis episodes by year-patients were 1,55 renal colics and 0.34 stone formation before phosphate treatment, versus 0.66 renal colics and 0.10 stone formation (more than 60% reduction), during treatment. There was simultaneously decrease of hypercalciuria (24 cases out of 42), of asthenia (16 cases out of 19), of signs of spasmophilia (12 cases out of 18) and disappearing of bone pains (4 cases out of 6). Side effects were rare. Minor digestive troubles were observed in 11 cases: diarrhea (3 cases) or gastralgias (9 cases). These side-effects necessitated discontinuation of thiazide therapy in only two cases and reduction of doses in 6 other cases. From our data, phosphate therapy appears an efficient drug in recurrent calcium nephrolithiasis. It acts in reducing levels of calciuria and enhancing urinary pyrophosphates excretion, inhibitors of calcium crystallization.

Adult↗