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PubMed2004

The metabolic syndrome and uric acid nephrolithiasis: novel features of renal manifestation of insulin resistance.

BACKGROUND: Uric acid nephrolithiasis primarily results from low urinary pH, which increases the concentration of the insoluble undissociated uric acid, causing formation of both uric acid and mixed uric acid/calcium oxalate stones. These patients have recently been described as exhibiting features of insulin resistance. This study was designed to evaluate if insulin resistance is associated with excessively low urinary pH in overtly healthy volunteers (non-stone formers) and if insulin resistance may explain the excessively low urinary pH in patients with uric acid nephrolithiasis. METHODS: Fifty-five healthy volunteers (non stone-formers) with a large range of body mass index and 13 patients with recurrent uric acid nephrolithiasis underwent hyperinsulinemic euglycemic clamp, 24-hour urinary studies, and anthropometric measurements of adiposity. A subgroup of 35 non-stone formers had 2-hour timed urinary collection before and during the hyperinsulinemic phase of the clamp studies. RESULTS: For the non-stone former population, low insulin sensitivity measured as glucose disposal rate significantly correlated with low 24-hour urinary pH (r= 0. 35; P= 0.01). In addition to the previously described acidic urine pH and hypouricosuria, patients with recurrent uric acid nephrolithiasis were found to be severely insulin resistant (glucose disposal rate: uric acid stone-formers vs. normals; 4.1 +/- 1.3 vs. 6.9 +/- 2.1 mg/min/kg of lean body mass, P= 0.008). Acute hyperinsulinemia was associated with higher urinary pH (6.1 +/- 0.7 at baseline to 6.8 +/- 0.7 during hyperinsulinemia; P < 0.0001), urinary ammonia excretion (2.7 +/- 1.6 mEq/2 hr at baseline and 4.0 +/- 2.6 mEq/2 hr P= 0.002) and urinary citrate excretion (48 +/- 33 mg/2 hr at baseline and 113 +/- 68 mg/2 hr P < 0.0001). CONCLUSION: We conclude that one renal manifestation of insulin resistance may be low urinary ammonium and pH. This defect can result in increased risk of uric acid precipitation despite normouricosuria.

Acids↗

PubMed2004

Association of urinary pH with body weight in nephrolithiasis.

BACKGROUND: The prevalence of kidney stone disease in the United States is progressively increasing, paralleling the growing rate of obesity. Uric acid nephrolithiasis, a condition associated with a low urinary pH, has been linked to obesity and insulin resistance. Based on these observations, we hypothesized that urinary pH may be inversely associated to body weight in nephrolithiasis. METHODS: Data were retrieved from 4883 patients with nephrolithiasis who underwent ambulatory evaluation at two established stone clinics in Dallas and Chicago. The patients collected 24-hour urine samples on an outpatient basis, while avoiding any drug that could alter urinary pH. Patients were divided in increasing sextiles of body weight, and urinary pH was adjusted for urinary creatinine and for age. RESULTS: Urinary pH had a strong, graded inverse association with body weight. Urinary creatinine and age were both found to be significant covariates of urinary pH, while gender was not a significant independent variable after adjustment for urinary creatinine. Mean 24-hour urinary pH, adjusted for age and urinary creatinine, were 6.09, 6.04, 6.01, 5.99, 5.97, and 5.91 for sextiles of body weight in increasing order from Dallas (P for linear trend <0.0001), and 6.18, 6.10, 6.04, 6.02, 5.97, and 5.88 for the sextiles from Chicago (P for linear trend <0.0001). CONCLUSION: We conclude that urinary pH is inversely related to body weight among patients with stones. The results confirm the previously proposed scheme that obesity may sometimes cause uric acid nephrolithiasis by producing excessively acid urine due to insulin resistance.

Adult↗

PubMed2004

Nephrolithiasis associated with ceftriaxone therapy: a prospective study in 51 children.

BACKGROUND: Ceftriaxone, a third generation cephalosporin, is widely used for treating infection during childhood. The kidneys eliminate approximately 33-67% of this agent, and the remainder is eliminated via the biliary system. Ceftriaxone may bind with calcium ions and form insoluble precipitate leading to biliary pseudolithiasis. The aim of this study was to assess whether ceftriaxone associated nephrolithiasis develops by the same mechanism, and whether this condition is dose related. METHODS: The study involved 51 children with various infections. Of these, 24 were hospitalized with severe infection and received 100 mg/kg/day ceftriaxone divided into two equal intravenous doses. The other 27 patients received a single daily intramuscular injection of 50 mg/kg/day. Serum and urine parameters were evaluated before and after treatment, and abdominal ultrasonographic examinations were also carried out before and after treatment. RESULTS: Serum urea, creatinine, and calcium levels were normal in all patients before and after treatment. Post-treatment ultrasound identified nephrolithiasis in four (7.8%) of the 51 subjects. The stones were all of small size (2 mm). Comparison of the groups with and without nephrolithiasis revealed no significant differences with respect to age, sex distribution, duration of treatment, or dose/route of administration of ceftriaxone. The renal stones disappeared spontaneously in three of the four cases, but were still present in one patient 7 months after ceftriaxone treatment. CONCLUSIONS: Conclusions: The study showed that children taking a 7 day course of normal or high dose ceftriaxone may develop small sized asymptomatic renal stones. The overall incidence of nephrolithiasis in this study was 7.8%.

Adolescent↗

PubMed2004

A review of the heritability of idiopathic nephrolithiasis.

Familial aggregations of nephrolithiasis were already noted in the early 19th century and over the intervening years there has been gradual progression in classifying the familial forms of nephrolithiasis. To date, there are at least 10 different monogenic conditions where those affected have a predisposition to nephrolithiasis. However, all of these rare conditions probably account for less than 2% of renal stone formers. This review, rather than considering these clearly defined disorders, concentrates on research into the broad band of stone formers who have a propensity to nephrolithiasis without an obvious discrete genetic basis.

Calcium↗

PubMed1994

Diet and nephrolithiasis.

Pharmacologic therapy of recurrent nephrolithiasis continues to be the mainstay of the strategy to prevent recurrence. This approach persists even in the face of increasing evidence of a marked benefit of mere entry into a nonpharmacologic diet and fluid modification protocol at a clinic specializing in the evaluation and therapy of recurrent nephrolithiasis (the "Stone Clinic effect"). This review examines the role of diet in the pathogenesis of various forms of nephrolithiasis and the effectiveness of dietary therapy in preventing new stone formation. Recent and older evidence support a primary role for modification of diet, particularly diet protein and sodium intake, in the prevention of recurrent nephrolithiasis.

Calcium↗

PubMed1985

Renal acidification defects in patients with recurrent calcium nephrolithiasis.

The frequency of renal tubular acidosis was evaluated in 28 adult patients with recurrent calcium nephrolithiasis (19 with 'renal' hypercalciuria, 9 with normocalciuria and no metabolic abnormality) and no evidence of obstruction or infection of the urinary tract. Eight patients with hypercalciuria (42%) had a defective renal reabsorption of bicarbonate, based on a fractional excretion of bicarbonate higher than 7% and a TmHCO3/GFR lower than 2.2 mEq/dl; 2 of them had an associated distal defect of acidification, as judged by a U-B pCO2 lower than 18 mm Hg in maximally alkaline urine. One patient with hypercalciuria had distal tubular acidosis, based on a urine pH higher than 5.3 during acidosis. Only 1 patient with normocalciuria had associated proximal and distal acidification defects. The remaining 8 patients displayed a normal renal acidifying capacity. The bicarbonate wastage was independent of serum PTH levels, vitamin D status and hypercalciuria and was associated with a defective tubular reabsorption of phosphate, increased random urinary pH and more active nephrolithiasis, with a prevalence of mixed calcium oxalate and phosphate stones. Our study shows a high incidence of defective tubular reabsorption of bicarbonate in patients with calcium nephrolithiasis and 'renal' hypercalciuria and suggests that the proximal acidification defect plays a pathogenetic role in promoting calcium nephrolithiasis.

Acidosis, Renal Tubular↗

PubMed1989

Comparative study of the circadian rhythmicity in the urinary concentration of glycosaminoglycans in patients of calcium oxalate nephrolithiasis and in healthy adults.

Glycosaminoglycans (GAGs) are potent inhibitors of calcium oxalate crystallisation and/or crystal aggregation. Urinary concentration of GAGs has been shown to vary during 24 h; therefore, circadian rhythmicity in urinary concentration of GAGs was investigated in 33 healthy male adults in the age group of 20-40 years and in 27 male patients of a similar age group with calcium nephrolithiasis. Three-hourly urine samples were collected for 24 h beginning from 00.00 h for estimation of urinary concentration of GAGs. The data of each patient was analysed by single cosinor rhythmometry and population mean-cosinor rhythmometry was then applied to each group. Twenty-four-hour urinary excretion of GAGs was significantly less in renal calculus patients (16.867 +/- 5.89 mumol) than in healthy subjects (22.588 +/- 5.32 mumol; p less than 0.001). A statistically validated circadian rhythm in urinary concentration of GAGs was demonstrated in both the groups. However, the amplitude-acrophase test revealed a significant difference between the two groups (F2,57 = 8.305; p less than 0.001); the amplitude was 2.354 mumol/l in patients with nephrolithiasis, whereas the amplitude was 7.028 mumol/l in healthy adults. The mesor test also revealed a significant difference in the 3-hour urinary concentration of GAGs between the two groups (18.536 mumol/l in healthy adults vs. 9.728 mumol/l in patients with nephrolithiasis). Thus in patients with nephrolithiasis, not only is the 24-hour urinary excretion of GAGs significantly low but the 3-hourly urinary concentration of GAGs is also significantly decreased as compared to healthy subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2003

Nephrolithiasis in Cushing's disease: prevalence, etiopathogenesis, and modification after disease cure.

The pathogenesis of nephrolithiasis in Cushing's syndrome is still not completely clarified. The current study aimed at investigating prevalence of nephrolithiasis and role of different lithogenic factors in Cushing's disease (CD). Forty-six CD patients (24 with active and 22 with cured disease) and 46 sex- and age-matched controls entered the study. Body mass index, blood pressure, fasting glucose and insulin, serum and urinary creatinine, urea, uric acid, electrolytes, and cystine, urinary volume, pH, oxalate, and citrate levels, and renal ultrasonography (US) were performed in all patients and controls. Nephrolithiasis was found in 50% of active patients, 27.3% of cured patients, and 6.5% of controls (P < 0.001). Compared with controls, patients with active disease had a significantly increased prevalence of obesity, arterial hypertension, diabetes mellitus, hypercalciuria, hypocitraturia, and hyperuricosuria, significantly higher levels of serum and urinary cystine, urinary creatinine, urea, uric acid, potassium, calcium, phosphorus, and oxalate, significantly lower levels of urinary citrate levels. Compared with controls, patients cured from CD had a significantly increased prevalence of obesity, systemic arterial hypertension, and diabetes mellitus, whereas urinary citrate was significantly decreased. At multivariate analysis, a significantly increased risk to develop kidney stones was independently associated with urinary excretion of uric acid (odds ratio = 1.6, confidence interval = 1.0-2.5) and systemic arterial blood pressure (odds ratio = 2.6, confidence interval = 1.1-6.6). In conclusion, patients with active CD have an increased prevalence of nephrolithiasis compared with general population, which decreases but not disappears in patients successfully cured from the disease. This complication is likely caused by the synergic effect of different hypercortisolism-dependent metabolic and hemodynamic abnormalities, among which systemic arterial hypertension and excessive urinary uric acid excretion seem to play a pivotal role.

Adult↗

PubMed2000

Increased prevalence and analysis of risk factors for indinavir nephrolithiasis.

PURPOSE: Indinavir is a protease inhibitor used for treating HIV-1. The drug is lithogenic and was thought to cause a 3% incidence of kidney stones. We evaluated a cohort of patients positive for HIV on indinavir to determine the incidence of indinavir nephrolithiasis and identify risk factors for indinavir stone formation. MATERIALS AND METHODS: Our cohort study of the prevalence of indinavir nephrolithiasis included 155 patients with HIV for 5,732 patient-weeks. The same cohort was then used for a retrospective chart review to assess patient age, weight, duration of drug use, time to stone formation, CD4 count, creatinine, alanine transaminase, and urinary pH and specific gravity as risk factors for stone formation. RESULTS: We estimated the cumulative incidence of indinavir stone formation by the Kaplan-Meier product limit estimator method. At 78 weeks 43.2% of patients had stones (95% confidence interval [CI] 0.292 to 0.543). Increasing age was the only variable that was a statistically significant predictor of indinavair urolithiasis (relative risk 0.955, 95% CI 0.918 to 0.993, p = 0.0159). The mean duration plus or minus standard deviation of indinavir use was statistically the same in each group (42.5 +/- 27. 2 and 40.3 +/- 27.1 weeks in those without and with stones, respectively) despite the observed mean time to stone formation of 23.0 +/- 19.8 weeks. CONCLUSIONS: The clinical prevalence of indinavir nephrolithiasis is much greater than initially reported. Nephrolithiasis during indinavir use does not appear to induce patients to withdraw from the drug.

Adult↗

PubMedDate not supplied

[Mineral water Volzhanka from Undorovskĭ spring in combined therapy of patients with nephrolithiasis and chronic pyelonephritis].

Water loading is an essential component in therapy of nephrolithiasis, especially in the presence of small ureteral concrements or fragments after extracorporeal shock-wave lithotripsy. Saluretics, furosemide in particular, cause side effects. One of these is dyselectrolytemia due to potassium loss. Mineral waters have advantages in the treatment of nephrolithiasis and pyelonephritis as their drinking does not lead to electrolyte loss. Low mineral waters are highly diuretic, e.g. after drinking 1 liter of Volzhanka day-time diuresis increases by 300-400 ml. This relieves ureteral and calyceal-pelvic tonicity stimulating elimination of the concrements or their fragments after lithotripsy. Intake of Volzhanka proved effective in combined therapy of nephrolithiasis, calculous pyelonephritis, urate nephrolithiasis.

Chronic Disease↗

PubMed2004

Sulfadiazine-induced nephrolithiasis detected by spiral CT scan.

Nephrolithiasis is a known complication of the use of sulfadiazine in the treatment of cerebral toxoplasmosis. Radiographic diagnosis of this complication has historically been challenging. Between March 1999 and June 2002, 11 patients were treated for cerebral toxoplasmosis with sulfadiazine-containing therapy. Four of these patients (36.4%) developed nephrolithiasis during this period. Case patients had received sulfadiazine for a median of 35.5 days prior to nephrolithiasis. All cases were diagnosed by spiral CT scans. Although studies are needed to evaluate the sensitivity and specificity of this modality, spiral CT may aid in the diagnosis of sulfadiazine-induced nephrolithiasis.

AIDS-Related Opportunistic Infections↗

PubMed1989

Effect of diclofenac-Na on 24-hour urinary excretion of creatinine, calcium, uric acid and glycosaminoglycans in adult patients with recurrent calcium oxalate nephrolithiasis.

Non-steroidal anti-inflammatory drugs (NSAID viz. indomethacin, flurbiprofen) decrease urinary calcium excretion in male Sprague-Dawley rats. Indomethacin decreases significantly the urinary calcium excretion in hypercalciuric patients. These observations encouraged the use of NSAID in the treatment of nephrolithiasis with encouraging initial results. However, NSAID (indomethacin and naproxen) retard both glycosaminoglycans (GAGs) synthesis and degradation thereby causing a significant reduction in the urinary excretion of GAGs, known to be potent inhibitors of calcium oxalate crystallization. Therefore, the effect of another NSAID, diclofenac-Na (50 mg t.i.d. for 4 weeks) was studied on 31 recurrent calcium oxalate nephrolithiasis patients who were not hypercalciuric or hyperuricosuric. The 24-h urinary excretion of creatinine, calcium and uric acid remained unchanged at 2 weeks and 4 weeks of therapy. However, after treatment of 2 weeks and 4 weeks, there was a significant decrease in the 24-h urinary excretion of GAGs (from 17.04 +/- 7.39 mumol to 11.54 +/- 7.02 and 12.7 +/- 6.2 mumol, respectively), and urinary concentration of GAGs (from 10.77 +/- 7.09 mumol/l to 6.03 +/- 5.00 mumol/l and 7.35 +/- 4.81 mumol/l, respectively). Thus diclofenac-Na (50 mg t.i.d.) did not reduce urinary excretion of calcium but significantly lowered the urinary excretion and concentration of GAGs in normocalciuric nephrolithiasis patients, an observation which cautions against the use of diclofenac-Na in prevention of nephrolithiasis in this group of patients.

Adult↗

PubMed1985

Bone mineral content in idiopathic calcium nephrolithiasis.

The calcium content of the central one third of the skeleton was measured using neutron activation analysis in 109 patients with idiopathic calcium nephrolithiasis. The bone mineral content (calcium bone index or CaBI, corrected for body size) was significantly decreased by 5.2% in 20- to 60-year-old patients with calcium nephrolithiasis (p less than 0.01). Under age 50 the decrease was more marked in 64 males (7.1%; p less than 0.02) than in 21 females (4.1%; p = NS). There was a significant negative correlation of CaBI with fasting urine calcium/creatinine ratio (r = 0.39; p less than 0.01), but no correlation with age or indices of parathyroid function. The decrease in bone mineral content did not appear to be progressive. The decrease in CaBI indicates negative calcium balance, either in the past or at present, in patients with calcium nephrolithiasis and does not favour increased intestinal absorption as a primary cause. The lack of correlation of CaBI with parameters of parathyroid function does not support a primary renal loss of calcium. The results suggest that increased bone turnover may be an important component of disordered calcium metabolism in patients with calcium nephrolithiasis.

Adult↗

PubMed1993

[Behavior of sex hormone and gonadotropin secretion in men with active nephrolithiasis].

Urinary excretion of calcium, magnesium, phosphate and oxalate in the condition of low-calcium diet, and the secretion of LH, FSH, testosterone and estradiol following LH-RH stimulation test have been determined in 26 men with active nephrolithiasis and in 14 healthy male subjects. Significantly higher urinary excretion of calcium and oxalate, and significantly lower excretion of magnesium was observed in men with nephrolithiasis as compared to healthy men. In addition, the patients with nephrolithiasis had significantly higher concentrations of testosterone, estradiol and FSH than the healthy controls. The results obtained suggest the participation of the gonadal hormones in the pathogenesis of active nephrolithiasis.

Adult↗

PubMedDate not supplied

[Risk factors for the occurrence of nephrolithiasis in the Aral Sea region].

The effects of environmental hazards on nephrolithiasis onset were studied for population of the regions exposed to ecological catastrophe sequelae by the sea Aral. Blood and urine levels of organic acids and trace elements were measured using chromato-mass spectrometry, absorption plasma spectrophotometry and ion-exchange chromatography, respectively, as well as urinary peptide hydrolases activity in 178 patients with nephrolithiasis. The levels of lithogenic substances in the blood and urine were distributed differently in patients living in different ecological zones. The above ecologically detrimental zones were denoted as zone 1--most distant from the Aral, zone 2--less distant from it and zone 3--the most ecologically damaged regions of the Aral catastrophe. The multivariate statistical analysis revealed factors of risk to develop nephrolithiasis for these zones: high and moderate risk was stated for 26%, 28.5% and 42.5% of the patients from zones 1, 2 and 3, respectively. The findings confirm the conception on an essential role of environmental factors in initiation of Aral-region nephrolithiasis.

Chromatography, Ion Exchange↗

PubMed1994

Studies on nephrolithiasis in patients with autosomal dominant polycystic kidney disease.

Eighty two patients with autosomal dominant polycystic kidney disease were examined clinically. Nephrolithiasis was diagnosed in 23 patients (28.1%). In 17 (73.5%) the lithiasis was bilateral. There were no patients with nephrolithiasis under the age of 20 years. The disease frequency increased in the patients between 21 and 40 years (38.5%) reaching 58.1% in those above 41 years. Nephrolithiasis in autosomal dominant polycystic kidney disease is not induced by the chronic renal failure. The opposite is more likely-nephrolithiasis precipitates the onset of renal failure. The autosomal dominant polycystic kidney disease is an etiologic factor for lithiasis.

Adolescent↗

PubMed2026

Comprehensive Landscape of Post-Translational Modification Alterations in Nephrolithiasis Revealing Activation of Multiple Cell Death Pathways.

Nephrolithiasis is a common urinary disorder characterized by high prevalence and recurrence, but the molecular mechanisms underlying calcium oxalate (CaOx)-crystal-induced renal injury remain incompletely understood. We applied integrated proteomic, phosphoproteomic, acetylomic, and lactylomic analyses to kidney tissues from a mouse model of CaOx nephrolithiasis followed by bioinformatic analysis and experimental validation. We identified 658 differentially expressed proteins, 735 differential phosphorylation sites, 335 differential acetylation sites, and 113 differential lactylation sites. Functional enrichment indicated immune activation, fibrotic remodeling, and alterations in PI3K-Akt, NOD-like receptor, p53, and Toll-like receptor signaling together with changes in fatty acid degradation, the tricarboxylic acid cycle, and glycolysis. Kinase activity prediction suggested the relative activation of multiple cyclin-dependent kinases. Proteins associated with ferroptosis, autophagy, necroptosis, and pyroptosis, including ACSL4, BNIP3, RIPK3, and GSDMD, showed coordinated abundance and modification changes. Several candidate sites, including MTOR_S1849, GCLM_K94, GCLM_S59, and GSS_K172, were also dysregulated. These data provide a multiomics resource for CaOx nephrolithiasis and identify candidate PTM events and regulatory pathways for future mechanistic validation.

Animals↗

PubMed2007

Ceftriaxone associated nephrolithiasis: a prospective study in 284 children.

Urinary tract calculi have been reported to account for between 1 in 1,000 and 1 in 7,600 hospital admissions in children in the USA. The annual incidence of urolithiasis in patients older than 10 years is 109 per 100,000 of the population in men and 36 per 100,000 of the population in women in Minnesota. The use of various medications is considered to be one of the etiologic factors of nephrolithiasis. Ceftriaxone is a widely used third-generation cephalosporin that is generally considered very safe, but complications such as biliary pseudolithiasis, and rarely, nephrolithiasis have been reported in children. There is limited information about urolithiasis as a side effect of ceftriaxone. The aim of this study was evaluation of the incidence of nephrolithiasis following ceftriaxone therapy in children. This quasi-experimental before and after study was conducted in Mofid Children's Hospital between 2003 and 2005. All patients were treated with 75 mg/kg intravenous ceftriaxone. Diagnosis of pyelonephritis was based on standard criteria. The first renal ultrasonography was performed on the first or second day of admission and was repeated on the last day of treatment. We also evaluated complicated patients for the third time with renal ultrasonography 3 months after treatment. Stone-forming patients underwent metabolic kidney stone risk factor evaluation. We evaluated 284 patients with pyelonephritis, 185 girls and 99 boys. The first ultrasonography was normal in all of our patients. On the second ultrasonography renal stones were reported in 4 out of 284 cases (1.4% and CI=0.96-1.83%). Underlying metabolic risk factors could not be identified in stone-forming patients. Follow-up ultrasonography 3 months later was normal. The results of our study suggest that ceftriaxone-treated patients may be at an increased risk of kidney stone formation. Stones passed spontaneously in all affected patients so the use of this effective drug can be safely continued. Close monitoring of ceftriaxone-treated patients with regard to kidney stone formation is recommended.

Anti-Bacterial Agents↗