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PubMed1994

Nephrolithiasis Clinical Guidelines Panel summary report on the management of staghorn calculi. The American Urological Association Nephrolithiasis Clinical Guidelines Panel.

The American Urological Association Nephrolithiasis Clinical Guidelines Panel recommendations for managing struvite staghorn calculi are based on a comprehensive review of the treatment literature and meta-analysis of outcome data from the 110 pertinent articles containing viable, unduplicated data. The panel concluded that the 3 most significant outcome probabilities are those of being stone-free, undergoing secondary unplanned procedures and having associated complications. Panel guideline recommendations for most standard patients are that neither shock wave lithotripsy monotherapy nor open surgery should be a first-line treatment choice but that a combination of percutaneous stone removal and shock wave lithotripsy should be used.

Humans↗
PubMed2005

Mapping a new suggestive gene locus for autosomal dominant nephrolithiasis to chromosome 9q33.2-q34.2 by total genome search for linkage.

BACKGROUND: Nephrolithiasis is a complex, multifactorial disease resulting from genetic and environmental interaction. The pathogenesis of nephrolithiasis is far from being understood. So far, no gene locus for autosomal dominant nephrolithiasis only has been described. We here identified a new suggestive gene locus for autosomal dominant nephrolithiasis by a genome-wide search for linkage in a Spanish kindred with nephrolithiasis. METHODS: Clinical data, blood and urine samples of 18 individuals from a Spanish kindred with nephrolithiasis were collected. We performed a genome-wide search for linkage using 380 polymorphic microsatellite markers. RESULTS: Nephrolithiasis segregated in this Spanish kindred in a pattern compatible with autosomal dominant inheritance. The total genome search yielded the highest two-point LOD score of Z(max) = 1.99 (theta = 0) for marker D9S159 on chromosome 9q33.2-q34.2. Multipoint analysis of 24 polymorphic markers used for further fine mapping resulted in a LOD score of Z(max) = 2.7 (theta = 0) for markers D9S1881-D9S164, thereby identifying a new gene locus for autosomal dominant nephrolithiasis (NPL1). Two recombination events define D9S1850 as the centromeric flanking marker and D9S1818 as the telomeric flanking marker, restricting the NPL1 locus to a 14 Mb interval. CONCLUSION: We here identified a new suggestive gene locus (NPL1) for autosomal dominant nephrolithiasis. It is localized on chromosome 9q33.2-q34.2. The identification of the responsible gene will provide new insights into the molecular basis of nephrolithiasis.

Aged↗
PubMed2000

Anatomic and metabolic risk factors for nephrolithiasis in patients with autosomal dominant polycystic kidney disease.

The prevalence of nephrolithiasis is considerably greater in patients with autosomal dominant polycystic kidney disease (ADPKD) than in the general population. We evaluated anatomic and metabolic factors that may be associated with an increased prevalence of nephrolithiasis in patients with ADPKD. We compared anatomic parameters among ADPKD patients with or without nephrolithiasis as diagnosed by ultrasonography, whereas metabolic factors were determined by 24-hour urinary chemical analysis. Patients with ADPKD and nephrolithiasis had more renal cysts (P < 0.05) and a larger predominant renal cyst size (P < 0.005) than patients without nephrolithiasis. Concurrently, individual stone-forming kidneys had a greater cyst number (P < 0.05) and a significantly larger predominant cyst size (P < 0.01) compared with kidneys without stones. Patients with ADPKD and nephrolithiasis had a significantly lower creatinine clearance than those without nephrolithiasis (68.7 +/- 8.6 versus 94.8 +/- 5.4 mL/min, respectively; P < 0.05). Twenty-four-hour urinary analysis showed that patients with ADPKD and nephrolithiasis had significantly lower urinary volumes (P < 0. 05), and levels of urinary phosphate (P < 0.05), magnesium (P < 0. 005), and potassium (P < 0.05). Although not statistically significant, patients with ADPKD with stones tended to have lower levels of urinary citrate, and both groups showed a high percentage (range, 49% to 60%) of patients with hypocitraturia. Our data are consistent with the hypothesis that patients with ADPKD who develop nephrolithiasis do so because of increased intrarenal anatomic obstruction, as well as lower levels of such urinary inhibitors of stones as magnesium and citrate.

Adult↗
PubMed1982

Increased risk of nephrolithiasis in patients with steatorrhea.

Patients with ileal disease have increased absorption of dietary oxalate, hyperoxaluria, and an increased incidence of nephrolithiasis. Patients with steatorrhea of varying etiologies also have hyperoxaluria. To determine whether steatorrhea per se is associated with nephrolithiasis, we reviewed the charts of all adult patients who had a 72-hr fecal fat analysis from 1968 to 1978. The 159 patients with steatorrhea were compared to 162 patients without steatorrhea. The two groups were comparable in age, sex, urine specific gravity, and serum uric acid and phosphorus; serum calcium was slightly less in the steatorrhea group (8.7 +/- 0.1 vs 9.0 +/- 0.1, P less than 0.02). Although 19 patients with steatorrhea had nephrolithiasis compared to 7 control patients (P = 0.01), 15 of these 19 patients had ileal disease and only 4 of the 118 patients with steatorrhea but without ileal disease had stones. Categorical data analysis revealed that steatorrhea, diarrhea (stool weight greater than 225 g/day), male sex, and ileal disease were significantly associated with nephrolithiasis with a relative risk of 3.0, 2.7, 3.1, and 8.0, respectively. When patients without ileal disease were analyzed separately, however, steatorrhea, diarrhea, and sex were no longer risk factors. In contrast, in patients with ileal disease the incidence of nephrolithiasis increased with the severity of steatorrhea. The relative risk of nephrolithiasis in male patients with ileal disease and fecal fat greater than 20 g/day was 26.3 (P less than 0.01). Thus, the presence of both ileal disease and steatorrhea greatly increases the risk of nephrolithiasis; however, neither steatorrhea alone nor ileal disease alone are risk factors for nephrolithiasis.

Celiac Disease↗
PubMed1998

Nephrolithiasis and risk of hypertension in women.

Cross-sectional and prospective studies of men suggest a positive association between nephrolithiasis and hypertension. However, this association remains controversial in women. We conducted a prospective study of the relation between nephrolithiasis and the risk for hypertension in the Nurses' Health Study, a cohort of 89,376 women aged 34 to 59 years in 1980. Information on the history of nephrolithiasis, physician-diagnosed hypertension, and other relevant exposures was obtained by biennial mailed questionnaire. A history of nephrolithiasis before 1980 was reported by 2,558 women (2.9%), and a history of hypertension was reported by 11,883 women (13.3%). Among women without hypertension before 1980, 12,540 women reported a new diagnosis of hypertension between 1980 and 1992, during 711,039 person-years of follow-up. Compared with those without a history of nephrolithiasis, the age-adjusted relative risk (RR) for incident hypertension in women with such a history was 1.36 (95% confidence interval [CI], 1.20 to 1.43). After further adjustment for body mass index (BMI) and the intake of calcium, sodium, potassium, magnesium, caffeine, and alcohol, the RR was only slightly attenuated (RR=1.24; 95% CI, 1.13 to 1.37). In contrast, the occurrence of incident nephrolithiasis during follow-up was similar in women with hypertension at baseline compared with women without (adjusted odds ratio [OR]=1.01; 95% CI, 0.85 to 1.20). These data are consistent with the results obtained in men and support the hypothesis that a history of nephrolithiasis is associated with an increased risk for subsequent hypertension. Dietary factors, such as the intake of calcium, sodium, and potassium, do not explain this association. Unidentified pathogenic mechanisms common to nephrolithiasis and hypertension may be responsible for the development of both disorders.

Adult↗
PubMed2000

Idiopathic hypercalciuria and hyperuricosuria: family prevalence of nephrolithiasis.

We studied the prevalence of a history of nephrolithiasis in first- and second-degree relatives of 74 children with hypercalciuria (HC), 61 with hyperuricosuria (HU), and 41 with HC plus HU, and in a control population of 261 children with different diseases. Family history of nephrolithiasis was found in 69% of HC, 75% of HU, 78% of HC plus HU, and 22% of control patients. The prevalence was not different among HC, HU, and HC plus HU groups, but was significantly higher in each study group than the control group (P=0.0001). Body mass index >95th percentile was found in only 4.7% of the patients with HC or HC plus HU. Calculi (>3 mm in diameter) were present in 8.9% of the patients with a family history of nephrolithiasis and in 9.4% of those with no family history (P=0.85). Microcalculi (<3 mm in diameter) were found by sonography in 56.6% of the patients with and in 53.3% of those without a family history of nephrolithiasis (P=0.83). Children with HC and/or HU have a strong familial prevalence of nephrolithiasis. Obesity does not seem to affect the association of familial nephrolithiasis and hypercalciuria in children. The presence of nephrolithiasis in families of children with HC and/or HU is not associated with a higher rate of formation of calculi or microcalculi.

Adolescent↗
PubMed1995

Ambulatory evaluation of nephrolithiasis: an update of a 1980 protocol.

Evaluations of 1,270 patients with recurrent nephrolithiasis in an outpatient setting were analyzed for the purpose of updating the classification of nephrolithiasis. All but 4% had abnormal urinary biochemistry that placed them into one or more of 20 etiologic categories. A single diagnosis was documented in 41.3% of patients. The remaining 58.7% had more than one diagnosis. Hypercalciuric calcium (Ca) nephrolithiasis, encountered in 60.9% of patients, comprised six variants--absorptive hypercalciuria Type I and II, renal hypercalciuria, primary hyperparathyroidism, and unclassified hypercalciuria (renal phosphate leak and fasting hypercalciuria). Hyperuricosuria Ca nephrolithiasis (HUCN) and gouty diathesis (GD) accounted for 35.8% and 10.0% of patients, respectively. Distinguishing features were hyperuricosuria and normal urinary pH in HUCN, and normal urinary uric acid and low urinary pH (< 5.5) in GD. Hyperoxaluric Ca nephrolithiasis, occurring in 8.1% of patients, was subdivided into enteric, primary, and dietary variants. Hypocitraturic Ca nephrolithiasis affected 28% of patients in its idiopathic variant. Many of these patients' problems were probably dietary in origin, while some could have had incomplete renal tubular acidosis. Hypocitraturia due to renal tubular acidosis or chronic diarrheal syndrome affected only 3.3% of patients. Hypomagnesiuric Ca nephrolithiasis, infection stones, and cystinuria were uncommon, accounting for 6.8%, 5.9%, and 0.9% of patients, respectively. The acquired problem of low urine volume (< 1 L/d) was found in 15.3% of patients. The remaining 3.5% of patients were difficult to classify despite the presence of abnormal urinary biochemistry.

Adult↗
PubMed2000

Symptomatic nephrolithiasis complicating pregnancy.

OBJECTIVE: To review our experiences with diagnosis and management of symptomatic nephrolithiasis complicating pregnancy and to ascertain the efficacy of renal sonography for initial diagnosis compared with plain x-rays or single-shot intravenous pyelography. METHODS: Perinatal outcomes were evaluated for all pregnant women admitted to Parkland Hospital for nephrolithiasis from 1986 to 1999. Diagnostic studies and management of nephrolithiasis were also evaluated. RESULTS: During the 13-year study period, 57 pregnant women had 73 admissions for symptomatic nephrolithiasis. Symptomatic nephrolithiasis complicated 1 in 3300 (0.03%) deliveries at our institution. Only 12 women (20%) had a history of renal calculi. Mean gestational age at diagnosis was 23 weeks. Imaging techniques included renal ultrasonography, plain abdominal x-ray, and single-shot intravenous pyelography. Calculi were visualized in 21 of 35 (60%) renal ultrasonographic examinations and 4 of 7 (57%) abdominal x-ray studies when these were performed as the initial test. In contrast, urolithiasis was discovered in 13 of 14 (93%) instances in which intravenous pyelography was performed as the initial diagnostic test. When sonography was negative (n = 14), renal calculi were confirmed by single-shot intravenous pyelography (n = 8). Although 43 of 57 (75%) of symptomatic episodes responded to conservative management, 10 women required ureteral stents, 3 needed percutaneous nephrostomy tubes, and 2 underwent ureteral laser lithotripsy for resolution. CONCLUSION: Although the convenience and safety of ultrasonography to initially diagnose nephrolithiasis are indisputable, 40% of calculi were missed when this method alone was used. Thus, if nephrolithiasis is still suspected clinically despite ultrasonographic findings, single-shot pyelography is recommended.

Adult↗
PubMed1998

Nephrolithiasis and risk of hypertension.

A positive association between nephrolithiasis and blood pressure has been suggested in previous studies. However, controversy remains, due to methodological problems in some of the previous studies and absence of prospective data. We evaluated the relationship between nephrolithiasis and the risk of hypertension in a cohort of 51,529 men followed prospectively for 8 years. Information was obtained by biennial mailed questionnaires. At baseline in 1986, 4111 (8.0%) subjects reported a history of nephrolithiasis and 11,623 (22.6%) a diagnosis of hypertension. A positive association was found between the two disorders (age adjusted odds ratio [OR]: 1.31; 95% confidence interval [CI]: 1.30 to 1.32). Among men who reported both disorders, 79.5% reported that the occurrence of nephrolithiasis was prior to or concomitant with the diagnosis of hypertension. Among men without hypertension at baseline, the odds ratio for incident hypertension in men with a history of nephrolithiasis compared with those without was 1.29 (95% CI: 1.12 to 1.41; adjusted for age, body mass index, and intake of calcium, sodium, potassium, magnesium, and alcohol). The occurrence of incident nephrolithiasis during follow-up was similar in men with hypertension at baseline compared with that in men without (adjusted OR: 0.99, 95% CI: 0.82 to 1.21). These data support the hypothesis that prior occurrence of nephrolithiasis increases the risk of subsequent hypertension.

Adult↗
PubMed2005

Direct and indirect costs of nephrolithiasis in an employed population: opportunity for disease management?

BACKGROUND: More than 5% of the United States population has been diagnosed with nephrolithiasis and about one half of (first-time) stone formers will have a recurrence within 5 years. The prevalence of nephrolithiasis is concentrated among working age adults, yet little prior work has examined the economic burden of the disease on employers and their employees. We sought to estimate the direct and indirect costs of nephrolithiasis for working age adults (18-64) with employer-provided insurance. METHODS: This was an observational study using retrospective claims data. Detailed medical and pharmacy claims from 25 large employers and absentee data from a subset of firms were used to estimate the direct and indirect costs associated with nephrolithiasis in a privately insured, non-elderly population. Multivariate regression models were used to predict health care expenditures for persons with and without the condition, controlling for differences in patient (health status) and plan characteristics. RESULTS: More than 1% of working-age adults were treated for nephrolithiasis in 2000. Prevalence was considerably higher among men and employees age 55 to 64. About one third of employees treated for nephrolithiasis in 2000 missed work due to the condition, with an average work loss for the entire treated population of 19 hours per person. Conditional on receiving treatment, the incremental costs of nephrolithiasis were 3,494 US dollars per person in 2000. CONCLUSION: The direct and indirect costs of nephrolithiaisis are substantial among working-age adults. Interventions that prevent recurrence among known stone formers may be a cost-effective component of disease management programs.

Adolescent↗
PubMed1990

Does medullary sponge kidney cause nephrolithiasis?

The prevalence of medullary sponge kidney in patients with nephrolithiasis and the issue of whether or not medullary sponge kidney has a role in the pathogenesis of renal stones are controversial. We studied the excretory urograms of 280 patients with nephrolithiasis and 280 patients without either nephrolithiasis or a history of renal stones to determine the frequencies of medullary sponge kidney in the two groups. The criterion for the diagnosis of medullary sponge kidney was the presence of a minimum of three linear or round collections of contrast material within one renal papilla. In the patients with nephrolithiasis, we also looked for biochemical evidence of metabolic causes of renal stones. The frequency of medullary sponge kidney was 12% in patients with nephrolithiasis compared with 1% in patients without nephrolithiasis. The statistical difference was highly significant (chi square = 27.1; p less than .001). Metabolic disorders accounting for the lithiasis were detected in 93% of the patients with stones without medullary sponge kidney. Such evidence was present in 60% of patients with stones and medullary sponge kidney. The statistical difference was significant (chi square = 25.8; p less than .001). Our results suggest that medullary sponge kidney is a cause of nephrolithiasis.

Adult↗
PubMed2001

Characterization of Tamm-Horsfall protein in a rat nephrolithiasis model.

PURPOSE: The role of Tamm-Horsfall protein in calcium oxalate stone formation is controversial. It is unclear whether Tamm-Horsfall protein has a role in crystallization. If it does, does it act as an inhibitor or promoter of crystallization? To elucidate the nature of its involvement we characterized Tamm-Horsfall protein in a rat model of calcium oxalate nephrolithiasis by in vivo and in vitro techniques. MATERIALS AND METHODS: Calcium oxalate nephrolithiasis was induced in male Sprague-Dawley rats. The amino acid and carbohydrate composition of Tamm-Horsfall protein from normal rats and those with nephrolithiasis was determined. The Tamm-Horsfall protein gene and protein expression in the kidneys were examined by in situ hybridization and immunohistochemistry. Furthermore, the interaction of Tamm-Horsfall protein and calcium oxalate crystals was assessed by an in vitro crystal aggregation assay. RESULTS: Tamm-Horsfall protein from rats with nephrolithiasis was biochemically similar to that from normal rats. Although Tamm-Horsfall protein was associated with crystal deposits in the renal papillae of rats with nephrolithiasis, Tamm-Horsfall protein messenger RNA expression in the kidneys remained unchanged. In each group Tamm-Horsfall protein inhibited calcium oxalate crystal aggregation by 47%, indicating no change in functional capabilities. CONCLUSIONS: The results of this study indicate that urinary excretion, and the biochemical nature and functional capabilities of Tamm-Horsfall protein remain unchanged during experimental calcium oxalate nephrolithiasis. Although staining for Tamm-Horsfall protein was evident in the papillae of rats with nephrolithiasis, the site of Tamm-Horsfall protein synthesis remained cells of the thick ascending limbs of the loop of Henle.

Animals↗
PubMedDate not supplied

[Role of physico-chemical and biochemical composition of urine in the genesis of combined nephrolithiasis and cholelithiasis].

Enzymuria, principal fractions of phospholipids, crystal-inhibiting urine activity were measured in 120 patients with nephrolithiasis combined with cholelithiasis. The patients were divided into two groups: group 1-80 patients with symptoms of nephrolithiasis and latent cholelithiasis; group 2-40 patients with symptoms of cholelithiasis and latent nephrolithiasis. It is shown that hyperenzymuria/microproteinuria, high excretion of phospholipids and cholesterol with urine in patients with nephrolithiasis and its complications not only affect physico-chemical properties of urine promoting atypical salt crystallization with stone formation but also determine characteristics of phasic urine conditions. High urine concentration of phospholipid (acyl derivatives) degradation products and cholesterol in patients with combination of nephrolithiasis with cholelithiasis changes solubilizing and micello-forming ability of urine and can directly stimulate crystal formation and development of aseptic inflammation in renal parenchyma. Low total crystal-inhibiting urine activity, altered surface-free energy due to surface-active substances, high calcium ionization and low urine magnesium ionization are not only pathognomonic criteria of nephrolithiasis but also parameters reflecting high risk of oxalate-calcium formation in patients with nephrolithiasis combination with cholelithiasis.

Adult↗
PubMedDate not supplied

Sodium dicarboxylate cotransporter-1 expression in renal tissues and its role in rat experimental nephrolithiasis.

BACKGROUND: Nephrolithiasis is a common disease with a high recurrence rate; however, calcium stone pathogenesis remains unknown because of complex multiple factors. Hypocitraturia induced by citrate transport disturbance is known to be involved in nephrolithiasis development. Sodium dicarboxylate cotransporter (NaDC) mediates citrate uptake from the renal proximal tubule. However, the role of NaDC in nephrolithiasis is unclear. This study aimed to investigate NaDC-1 expression in rat renal proximal tubule epithelial cells and its relationship with experimental nephrolithiasis. METHODS: Male Wastar rats were divided into control, ethylene glycol (EG)-treated and potassium citrate-treated groups. Calcium oxalate (CaOx) crystal deposition and histological changes in the kidneys were examined with anatomical and light microscopes. The plasma and urinary biochemical parameters, such as citrate, oxalate etc, were analyzed by routine biochemical methods. NaDC-1 mRNA expression in kidneys was determined by northern blot analysis, the change in NaDC-1 protein abundance was detected by immunohistochemistry. RESULTS: It was found that NaDC-1 expression and its mRNA significantly increased in the EG group when compared with controls. Increased NaDC-1 expression was associated with a decline in urinary citrate excretion. Potassium citrate administration could significantly down-regulate NaDC-1 expression and its mRNA, and elevate urinary citrate content alleviate renal pathological changes and reduce nephrolithiasis occurrence. CONCLUSION: Increased NaDC-1 expression on the renal proximal tubule epithelial cells could play an important role in nephrolithiasis development, suggesting it could be a therapeutic target for the treatment of nephrolithiasis.

Animals↗
PubMed2007

Management of nephrolithiasis after Cohen cross-trigonal and Glenn-Anderson advancement ureteroneocystostomy.

PURPOSE: Ureteroneocystotomy is frequently performed for ureteral injury or vesicoureteral reflux. The Glenn-Anderson technique advances the ureteral orifice distal to its native position, while the Cohen technique crosses the orifice to the opposite trigone. Each treatment can alter access to the upper genitourinary tracts. We report our experience with subsequent nephrolithiasis in these patients. MATERIALS AND METHODS: We performed a retrospective chart review of all patients treated with ureteroneocystotomy since 1980 who had nephrolithiasis. RESULTS: Nephrolithiasis developed in 9 patients with prior Cohen ureteroneocystotomy and in 15 with prior Glenn-Anderson ureteroneocystotomy. Stones size was 2 to 20 mm (mean 6.4). In the Cohen group ureteroscopy was attempted and failed in 2 patients, requiring percutaneous nephrolithotomy. Attempted shock wave lithotripsy failed in 2 patients, of whom 1 required percutaneous nephrolithotomy and 1 required observation. Primary percutaneous nephrolithotomy was performed in 1 patient. One patient required nephrectomy for chronic pyelonephritis related to nephrolithiasis. Two patients had active stone disease and were awaiting further treatment, while 1 passed the stone. In the Glenn-Anderson group ureteroscopy was successful in all 4 attempts. Attempted shock wave lithotripsy in 2 patients was successful in 1. The other patient required subsequent percutaneous nephrolithotomy. Primary percutaneous nephrolithotomy was required in 2 patients. All other patients were asymptomatic and under observation. CONCLUSIONS: Treatment for upper tract nephrolithiasis is effected by prior ureteroneocystotomy. Minimally invasive treatments were less successful after Cohen ureteroneocystotomy than after Glenn-Anderson ureteroneocystotomy. In this study patients with prior cross-trigonal ureteroneocystotomy required more invasive therapies for symptomatic nephrolithiasis.

Adolescent↗