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At least 271 records · Page 15Linked to original sources

PubMed2006

Changes in nitric oxide production in the rat kidney due to CaOx nephrolithiasis.

AIMS: The aim of the study was to test the hypothesis that the renal nitric oxide (NO) system is involved in the animal model of nephrolithiasis by evaluating the relationship between nitric oxide synthase (NOS) and oxidative stress. METHODS: Deposition of renal calculi was induced by adding 0.75% ethylene glycol (EG) to the drinking water of male Wistar rats. After 42 days of treatment, urinary biochemistry and urinary levels of oxalate, NO metabolites (nitrate and nitrite), cGMP, and lipid peroxides, and markers for renal damage and oxidative stress in the kidney were examined. In the second part of the experiment, two diuretic stimuli (intrarenal infusion of l-arginine or saline loading) were applied to test the renal NO system response. Finally, levels of three isoforms of NOS in renal tissues were evaluated by immunostaining. RESULTS: In the EG-treated rats, increased urinary excretion of enzymes and lipid peroxides and increased nitrotyrosine levels and oxidative injury markers in the kidneys indicated that peroxynitrite formation occurred during oxidative stress, while the 24-hr urinary excretion of NO metabolites and cGMP remained unchanged. In contrast to control rats, urinary excretion and NO metabolites and cGMP excretion were unresponsive to intrarenal l-arginine infusion; in response to saline loading, an increase in these factors was seen, but the increase was only 50% of that seen in the identically treated control group. A significant decrease in eNOS expression and increase in iNOS expression were observed in the renal medulla of the EG-treated group, whereas expression of nNOS was not affected. CONCLUSIONS: Although basal renal NO production remained unchanged, excessive peroxynitrite formation in the kidney was noted in this model. A decreased response of the NOS system was noted when diuretic stimuli were applied. How the imbalance between eNOS and iNOS expression influences CaOx stone formation requires detailed evaluation.

Animals↗

PubMed1994

Ammonium urate nephrolithiasis in a variant of Bartter's syndrome with intact renal tubular function.

In two patients with Bartter's syndrome proximal tubular function and distal chloride reabsorption were intact on admission; however, chloride reabsorption and distal tubular acidifying capacity decreased in one patient over a period of 10 years. Renal prostaglandin E excretion and urinary and plasma uric acid were in the normal range, but urinary ammonium was significantly elevated during controlled diet. One patient developed ammonium urate nephrolithiasis. In both patients renal biopsy demonstrated lymphocytic infiltration of the interstitial tissue and hypercellularity of the macula densa. Indomethacin treatment improved serum potassium concentration and decreased plasma renin activity, plasma aldosterone concentration, and urinary prostaglandin E but had to be discontinued because of side effects. It is likely that our patients represent a variant form of the syndrome originally described by Bartter.

Adult↗

PubMed1992

Correlation between 1.25 dihydroxyvitamin D serum levels and fractional rate of intestinal calcium absorption in hypercalciuric nephrolithiasis. Role of phosphate.

Different mechanisms could explain the elevated calcium elimination, the main cause of calcium oxalate renal stones. Our results suggest that phosphate levels are decreased in patients with absorptive hypercalciuric nephrolithiasis and elevated serum dihydroxyvitamin D. This could be the reason why in this group of patients oral phosphate treatment prevented hypercalciuria and renal lithiasis.

Calcitriol↗

PubMed1989

Hypercalciuria and nephrolithiasis as a presenting sign in Wilson disease.

A 9-year-old boy presented with recurrent episodes of renal colic. One year later Wilson disease was diagnosed. Evaluation of liver function and assessment of serum copper, caeruloplasmin concentration and urinary copper excretion in any child presenting with nephrolithiasis is suggested.

Calcium↗

PubMed1997

Expression of heparan sulfate proteoglycan mRNA in rat kidneys during calcium oxalate nephrolithiasis.

This study used reverse transcription polymerase chain reaction (RT-PCR) to examine heparan sulfate proteoglycan (HS-PG) mRNA expression levels during stone formation in the rat kidney. Total RNA in kidneys was extracted and converted to cDNA. PCR products were resolved by electrophoresis on 1.5% agarose gel and visualized with ethidium bromide. Fragment intensity and area were measured using an image analyzer. Control cyclophilin and HS-PG mRNAs were expressed in all samples examined as 235 bp and 506 bp bands, respectively. Cyclophilin expression in the normal group was not significantly different from expression in the group that formed stones. However, the level of HS-PG mRNA expression apparently increased in calcium oxalate (CaOx) microlith. The findings suggest an association between CaOx nephrolithiasis and expression of HS-PG in the rat kidney.

Animals↗

PubMed1980

[Parathormone and renal excretion in healthy controls and patients with nephrolithiasis (author's transl)].

Idiopathic nephrolithiasis with recurrent ca-oxalat stones are investigated for occult renal dysfunction or for disturbed clearance of PTH. After injection of PTE a significant increase of renal excretion of Na+, K+, Ca2+ and uric acid was observed normalizing within 120 min after injection. Healthy controls showed similar changes, and following PTH the cAMP generating capacity of patients with recurrent stones was in normal range. The turn over rate of PTH was 30-40 min without differences in the collectives studied.

Calcium↗

PubMed1991

Coexisting nephrolithiasis and cholelithiasis in premature infants.

Though the coexistence of nephrolithiasis and cholelithiasis in premature infants is extremely rare, we report four patients seen in a two year period. All patients weighed less than 1100 grams at birth, developed severe bronchopulmonary dysplasia, and all had Grade III or IV bilateral intraventricular hemorrhages. All four infants received prolonged furosemide therapy lasting at least 28 consecutive days. The renal stones disappeared in all four upon cessation of therapy, while in none have the gallstones disappeared after a mean follow-up period of 13 months. Ultrasound was superior in identifying and monitoring these stones. Their presence resulted in manipulating diuretic therapy which then was shown to limit renal and possibly biliary complications.

Bronchopulmonary Dysplasia↗

PubMed1985

Diagnostic value of urinary cyclic AMP measurement in patients with calcium nephrolithiasis.

One hundred patients with recurrent calcium nephrolithiasis were submitted to the Pak test. At fasting state hypercalciuria was found in 27 cases, while a group of 16 further patients became hypercalciuric after oral calcium load. Only measurement of urinary cAMP excretion in both conditions made it possible to diagnose renal hypercalciuria in 9 out of 27 patients in the former group; according to test results 4 patients were expected to have primary hyperparathyroidism, but afterwards the disease was identified in only one case.

Administration, Oral↗

PubMed2004

[Prevention of nephrolithiasis. Established strategies and new concepts].

During the last 2 decades in Germany, only minor efforts were expended for the prevention of urinary stones. Substantial technical progress simplified the treatment of existing calculi; thus, it was more convenient to treat a new stone than to prevent its recurrence. But times change! In these days of financial squeeze in the medical system, prevention becomes more attractive. Nevertheless, strategies for kidney stone prevention developed. Established concepts for dietary advice were rejected due to the results of new randomized studies. Moreover, new pharmacological substances were introduced for metaphyalxis. The new concepts are feasible for the daily routine. For some treatment modalities in stone prevention, there is valid evidence from the literature, which should encourage us to adopt these modalities in the future. A number of drugs are used as "good common practice" without any proof from a randomized trial. Often prospective and valid studies are not available. The present paper intends to describe the status quo of nephrolithiasis prevention in Germany, focussing on confirmed data and unsolved problems.

Captopril↗

PubMed2005

Nephrolithiasis complicating treatment of diabetes insipidus.

A decrease in urine volume is considered the therapeutic goal of the treatment of central diabetes insipidus (DI) with desmopressin (dDAVP). A low urine volume is a risk factor for kidney stone formation. This is the first report of nephrolithiasis in association with DI. It is likely that successful therapy with dDAVP and the patient's own purposeful decreased fluid intake contributed to calcium oxalate stone formation. Prevention of stone recurrence requires an increase in urine volume. The patient's compliance with this recommendation led to an episode of acute hyponatremia, a well-known complication of dDAVP therapy. The challenge of the management of stones in the setting of DI requires balancing the conflicting goals of both decreasing and increasing urine volume.

Adult↗

PubMed2002

Nephrolithiasis in a neonate with transient renal wasting of calcium and magnesium.

Following an uneventful full-term pregnancy, a 3-day-old girl presented with a focal seizure. Serological evaluation revealed hypomagnesemia and hypocalcemia. Renal ultrasonography performed because of hematuria showed bilateral nephrolithiasis. Renal wasting of calcium and magnesium was detected and urine citrate excretion was low. The hypocalcemia was refractory to calcium therapy, but responded briskly to magnesium supplementation. After 8 weeks of treatment with magnesium and calcium supplementation plus potassium citrate, the hypomagnesemia and hypocalcemia normalized spontaneously, as did the urinary calcium, magnesium, and citrate excretion. We speculate that our patient had a transient tubular defect in the thick ascending loop of Henle.

Calcium↗

PubMed2004

Sulfadiazine-induced nephrolithiasis in children.

Sulfadiazine-associated urinary calculi have been described in HIV-positive adult patients but rarely in children. We report two pediatric cases of sulfadiazine-induced nephrolithiasis and review 45 adult cases from the literature. One had a hyper-IgM syndrome and was treated with sulfadiazine for cerebral toxoplasmosis, the other had toxoplasmic retinitis. Both developed multiple bilateral lithiasis with acute renal failure. Normalization of renal function and reduction of calculi size was rapidly achieved after discontinuation of sulfadiazine, hyperhydration, and alkalinization. Bilateral ureteral stents were required in one patient because of anuria.

Adolescent↗

PubMed2005

Nephrolithiasis in children.

A metabolic etiology is the most common cause for pediatric kidney stones. Appropriate evaluation of affected children should include assessment of stone type, if available, and assessment of predisposing factors in all cases. This review discusses the metabolic disorders that lead to nephrolithiasis with respect to the development of calcium, uric acid, struvite, and cystine stones. Environmental and hereditary factors are summarized to provide a guide in the evaluation of pediatric stone formers.

Calcium↗

PubMed1996

Urinary inhibitors of crystallization in hypercalciuric children with hematuria and nephrolithiasis.

Urinary inhibitors are suggested to play a significant role in reducing crystallization in calcium (Ca) stone former and idiopathic hypercalciuria (IH). Urinary inhibitors such as magnesium (Mg), citrate, and glycosaminoglycans (GAGs) were evaluated, as well as urinary Ca and creatinine (Cr), in IH children with nephrolithiasis (LIT) or with hematuria plus IH (HEM) and were compared with a control group. The mean 24-h urinary excretion of Mg was similar in all groups. However, the urine Ca/Mg ratio was significantly increased (P < 0.005) in LIT and HEM groups. A higher mean value for GAGs and citrate was found in the HEM group, but a very low level of GAGs (less than 60% of the normal value) and citrate (less than 30% of the normal value) was found in the LIT group. These data suggest that, despite a high urinary Ca excretion (3.6 +/- 0.1 mg/kg per day) in the HEM group, elevated urinary GAGs (32.0 +/- 1.0 mg/g Cr) and a normal urinary citrate (428.7 +/- 62.3 mg/24 h) excretion may prevent Ca crystallization and thus renal stones. In contrast, in the LIT group low urinary GAG (10.3 +/- 0.9 mg/g Cr) and citrate (235.2 +/- 52.3 mg/24 h) excretion may precipitate stone formation in the presence of a high urinary Ca excretion. Thus, it is reasonable to suggest that patients with hematuria and IH may not develop overt renal stone due to the presence of normal levels of renal stone inhibitors.

Calcium↗

PubMed2004

Gestational urinary hyperthiosulfaturia protects hypercalciuric normal pregnant women from nephrolithiasis.

Urinary calcium excretion increases by 1-2-fold during gestation in normal, uncomplicated pregnant women. Hypercalciuria occurs in all trimesters and elevates urine supersaturation with regards to calcium oxalate. However, crystalluria has not been a frequent clinical finding and stone formation is not a common complication of pregnancy. To elucidate this discrepancy we measured various chemical entities (i.e. calcium, oxalate, uric acid, phosphorous, magnesium, citrate, sulfate and thiosulfate) in urine at the end of each trimester of 25 pregnant women. Twenty-five healthy women served as controls. Our observations show that endogenous thiosulfate, a natural component of urine, increased considerably during pregnancy to approximately 36, 38 and 40 microM/24 hour at the end of each three trimesters. One month after delivery, endogenous thiosulfaturia and hypercalciuria, in parallel, returned to initial normal values. Consequently, it seems that gestational hyperthiosulfaturia protects hypercalciuric normal pregnant women from the risk of nephrolithiasis.

Adult↗

PubMed1980

Ambulatory evaluation of nephrolithiasis. Classification, clinical presentation and diagnostic criteria.

Using the ambulatory protocol previously described, 241 patients with nephrolithiasis were evaluated. They could be categorized into 10 groups from the results obtained. Absorptive hypercalciuria type I (87 per cent male) comprised 24.5 per cent and was characterized by normocalcemia, normal fasting urinary calcium (less than 0.11 mg/100 ml glomerular filtration), an exaggerated urinary calcium following an oral calcium load (greater than 0.20 mg/mg creatinine), normal urinary cyclic adenosine monophosphate (AMP) (less than 5.4 nmol/100 ml glomerular filtration) and serum parathyroid hormone (PTH), and hypercalciuria (greater than 200 mg/day during a calcium- and sodium-restricted diet). Absorptive hypercalciuria type II (50 per cent male) accounted for 29.8 per cent; its biochemical features were the same as those for absorptive hypercalciuria type I, except for normocalciuria during a restricted diet and low urine volume (1.42 +/- 0.55 SD liter/day). Renal hypercalciuria (56 per cent male), disclosed in 8.3 per cent, was represented by normocalcemia and high values for fasting urinary calcium (0.160 +/- 0.054 mg/100 ml glomerular filtration), urinary cyclic AMP (6.80 +/- 2.10 nmol/100 ml glomerular filtration) and serum PTH. Primary hyperparathyroidism (57 per cent female), accounted for 5.8 per cent, typically included hypercalcemia, hypophosphatemia, hypercalciuria and high urinary cyclic AMP. Hyperuricosuric calcium urolithiasis (100 per cent male) comprised 8.7 per cent, and was characterized by hyperuricosuria (776 +/- 164 mg/day) and urinary pH exceeding pK for uric acid (5.91 +/- 0.33). In enteric hyperoxaluria (60 per cent female), encountered in 2.1 per cent of cases, urinary oxalate was increased (6.29 +/- 13.2 mg/day). Noncalcium-containing stones were found in 2.1 per cent of the patients with uric acid lithiasis (100 per cent male) and in another 2.1 per cent of the patients with infection lithiasis (60 per cent female). These conditions were typified by low urinary pH (5.29 +/- 0.12) and high urinary pH (6.69 +/- 1.16), respectively. Renal tubular acidosis was found in one patient (male, 0.4 per cent). In 10.8 per cent of the patients (81 per cent male), no metabolic abnormality could be found, although urine volume was low (1.41 +/- 0.51 liter/day). Hypercalciuria could not be differentiated between absorptive hypercalciuria and renal hypercalciuria in 5.4 per cent of the patients. Thus, this ambulatory protocol disclosed a physiologic disturbance in nearly 90 per cent of the cases and provided a definitive diagnosis in 95 per cent of the patients.

Adult↗

PubMed1982

Factors that predict relapse of calcium nephrolithiasis during treatment: a prospective study.

We evaluated 522 patients with idiopathic, recurrent calcium nephrolithiasis using a comprehensive clinical and laboratory protocol, and obtained additional laboratory measurements during their subsequent years of treatment in our program. In 57 patients, a new calcium stone ultimately formed during treatment (relapse), whereas 189 others have been free of recurrence during at least two years (average 4.3 +/- 2.2 [SD] years) of follow-up. Compared with the patients who remained stone-free, the patients with relapse (1) had a shorter interval between the time they entered our program and the time their last recurrent, pretreatment stone formed; (2) excreted more calcium *in mg/kg of body weight pr 24 hours) in their urine during treatment (2.79 +/- 1.08 versus 2.39 +/- 0.98 [SD] for relapse and stone-free); and (3) increased their urine volume less during treatment compared with pretreatment values (delta in liters per 24 hours was -0.02 +/- 0.48 versus 0.23 +/- 0.54 for relapse and stone-free). The two groups were otherwise the same. All comparisons used only data obtained prior to relapse. A discriminant function using only these three characteristics correctly identified 72 percent of patients with relapse and 67 percent of those who remained stone-free.

Allopurinol↗

PubMed1988

Uric acid nephrolithiasis and acute renal failure secondary to streptozotocin nephrotoxicity.

Uric acid nephrolithiasis developed in a 75-year-old man who had received a large cumulative dose of streptozotocin for treatment of metastatic islet cell carcinoma of the pancreas. Oligoanuric renal failure mediated by massive intraureteral uric acid deposits occurred despite normal serum concentrations of uric acid. This case implicates the uricosuric effects of streptozotocin in the pathogenesis of uric acid nephropathy and suggests that renal uric acid excretion should be monitored routinely in patients receiving large cumulative doses of this drug.

Acute Kidney Injury↗