[The treatment of nephrolithiasis of doubled kidney and of the upper urinary tract].
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The clinical and laboratory findings in 14 infants, 2 children and 42 adults with RTA-1 have been retrospectively analyzed and the patients classified as having the hereditary (14%), acquired (31%), or idiopathic (55%) form. In 7 of the 8 hereditary cases, RTA-1 appeared to be a complication of hereditary hypercalciuria. The majority of acquired cases (61%) were secondary to immune-mediated diseases. All of the 14 infants with RTA-1 were classified as idiopathic. All of the idiopathic cases in children and adults were associated with nephrolithiasis and/or nephrocalcinosis, 33% of which had a family history of nephrolithiasis. The 14 infants presented with failure to thrive. Seventy-seven percent of children and adults with RTA-1 had nephrolithiasis and/or nephrocalcinosis and usually presented with symptoms related to this problem. Adults without nephrolithiasis or nephrocalcinosis usually presented with electrolyte disturbances or acidosis. Hypokalemia, the most common electrolyte disturbance, was present in 28% of the entire series. Acidosis was present in all infants and in 70% of children and adults. Clinically apparent bone disease was observed in 3 infants, and in 1 adult with nephrolithiasis. Glomerular function was normal in infants and in the 2 children, but depressed in 40% of adults. Recurrent urinary tract infection was a contributing factor but was not the sole cause of renal failure. Surprisingly, kidney stone number, the number of surgical procedures, and the presence of nephrocalcinosis had no apparent effect on the development of renal failure. Glomerular filtration rate was significantly higher in patients with incomplete RTA-1, and serum total CO2 was significantly correlated with creatinine clearance and minimum urinary pH. Hypercalciuria was present in 32% of patients with nephrolithiasis and/or nephrocalcinosis, and urinary citrate excretion was low in all of 16 patients in whom it was measured. Hypocitraturia appeared to be due in most cases to potassium depletion and renal failure, but may have occurred as a primary defect in 1 patient with hereditary RTA. Urinary uric acid excretion was elevated in 23% of patients with stones in whom it was measured. The mean number of stone-forming events was 51 +/- 14. Although a weak correlation between urinary calcium excretion and stone number was observed, the cause for prodigious stone formation could not be explained. This series emphasizes the variable degree to which the common clinical manifestations of RTA-1 (metabolic acidosis, hypercalciuria, nephrolithiasis, nephrocalcinosis, and potassium depletion) are expressed.(ABSTRACT TRUNCATED AT 400 WORDS)
PURPOSE: Cystic fibrosis is characterized by chronic pulmonary disease, insufficient pancreatic and digestive function, and abnormal sweat concentrations. Patients with cystic fibrosis also have an increased incidence of nephrolithiasis. We compared the results of metabolic evaluation in patients with cystic fibrosis with and without nephrolithiasis. MATERIALS AND METHODS: A total of 496 patients were evaluated at our center, including 98 with a mean age of 25 years who had cystic fibrosis and complete metabolic evaluation available between 1996 and 2000. Of these patients 13 (13%) had a history of nephrolithiasis. The records were reviewed for clinical characteristics and all patients underwent metabolic evaluation, including serum electrolyte measurement and 24-hour urine collection. Statistical analysis was done to compare the stone versus nonstone groups. RESULTS: The incidence of nephrolithiasis in our study was 3%. We identified 13 patients 16 to 41 years old (mean age 27) with nephrolithiasis, of whom 62% had had multiple episodes. Flank pain was the presenting symptom in 9 of the 13 cases (69%). Renal ultrasound and computerized tomography were the most common imaging modalities. In 9 cases stones were passed without intervention, extracorporeal shock wave lithotripsy was required in 2 and ureteroscopy with stone extraction was done in 2. Calcium oxalate was the dominant stone composition in the 9 patients in whom stone analysis was performed. Metabolic evaluation of the stone versus no stone groups showed elevated urinary oxalate (45.5 versus 42.5 mg./24 hours), relative calcium oxalate supersaturation (5.3 versus 7.2) and decreased urinary citrate in the 2 groups. There was a statistical difference in citrate excretion with lower levels in stone formers (102 versus 218 mg./24 hours, p = 0.0007). CONCLUSIONS: Patients with cystic fibrosis have an increased incidence of nephrolithiasis and are at high risk for recurrence. Metabolic evaluation is indicated in all patients with cystic fibrosis and urolithiasis since most have hyperoxaluria, urinary calcium oxalate supersaturation and decreased urinary citrate. Correcting detected stone risk factors in these cases may decrease stone recurrence.
BACKGROUND AND PURPOSE: Recent studies have demonstrated a higher incidence of nephrolithiasis in the morbidly obese. Nephrolithiasis also has been described as a potential outcome after gastric bypass surgery. This is the first study to our knowledge that examines the incidence of nephrolithiasis in the morbidly obese in the setting of gastric bypass surgery at a tertiary referral center. PATIENTS AND METHODS: We retrospectively reviewed the records of patients undergoing laparoscopic gastric Roux-en-Y bypass surgery for morbid obesity at our institution for the incidence of nephrolithiasis preoperatively, de novo stones postoperatively, and both preoperative and postoperative stone formation. RESULTS: Of the 972 patients who underwent a laparoscopic gastric bypass for the treatment of morbid obesity between 1990 and the present, 85 (8.8%) were found to have upper urinary-tract calculi preoperatively, and 32 (3.2%) had de novo stones postoperatively. Of those 85 who had stones preoperatively, 26 (31.4%) developed recurrent stones postoperatively. CONCLUSIONS: These results support findings in the current literature that nephrolithiasis has a higher incidence in the morbidly obese population. The combination of preoperative stone history and gastric bypass surgery may place patients at a higher risk of future stone formation. This latter group of patients should be screened for postoperative stone formation.
Data are presented on 97 patients with primary hyperparathyroidism who constitute a representative cohort of the disease seen today. The average calcium (11.1 +/- 0.1 mg/dl; normal 8.7-10.7), phosphorus (2.8 +/- 0.1 mg/dl; normal 2.5-4.5), and parathyroid hormone level by immunoradiometric assay (119 +/- 7 pg/ml; normal 10-65) are typical of the modern presentation of primary hyperparathyroidism. Most patients were asymptomatic in that there was evidence for nephrolithiasis in only 18% and for radiologically evident bone disease in only 1% of patients. Nevertheless, when patients were evaluated with bone densitometry and with histomorphometric analysis of the bone biopsy specimen, evidence for the hyperparathyroid process could be shown in the majority of patients. Selective reduction of cortical bone and preservation of cancellous bone were apparent. Among patients with nephrolithiasis, no particular feature distinguished them from patients without nephrolithiasis. All biochemical data were similar between both stone and non-stone formers. The selective reduction in cortical bone was seen to the same extent among those with stones as among those without stones. The average 1,25-dihydroxyvitamin D level was not increased among those with stones. When the population was divided into groups with elevated or normal 1,25-dihydroxyvitamin D levels, the incidence of nephrolithiasis was unchanged. The results indicate that bone involvement can be demonstrated among most patients with asymptomatic primary hyperparathyroidism and that no pathophysiologic mechanisms are yet apparent to account for nephrolithiasis in primary hyperparathyroidism.
Calcific kidney stones in both humans and mildly hyperoxaluric rats are located on renal papillary surfaces and consist of an organic matrix and crystals of calcium oxalate and/or calcium phosphate. The matrix is intimately associated with the crystals and contains substances that can promote as well as inhibit calcification. Osteopontin, Tamm-Horsfall protein, bikunin, and prothrombin fragment 1 have been identified in matrices of both human and rat stones. Hyperoxaluria can provoke calcium oxalate nephrolithiasis in both humans and rats. Kidney-stone-forming rats are hypomagnesuric and hypocitraturic during nephrolithiasis. Human stone formers may have the same disorders. Males of both species are prone to develop calcium oxalate nephrolithiasis, whereas females tend to form calcium phosphate stones. Oxalate metabolism is considered to be almost identical between rats and humans. Thus, there are many similarities between experimental nephrolithiasis induced in rats and human kidney-stone formation, and a rat model of calcium oxalate nephrolithiasis can be used to investigate the mechanisms involved in human kidney stone formation.
UNLABELLED: We have sometimes encountered intractable cases of nephrolithiasis, even though ESWL and endourology have dramatically developed at the present time. We could obtain satisfactory result in the treatment of intractable right nephrolithiasis with ureterocalicostomy. CASE: The patient was a 39-year-old man having undergone PNL, ESWL, pyelolithotomy for right nephrolithiasis. Ten-odd stones, measuring 5-20 mm in diameter, were detected, and his IVP revealed mild hydronephrosis with the ureteropelvic junction stenosis. Pyeloplasty was thought to be difficult to perform. Thus the stones were removed through an incision made on the lowermost portion of the kidney followed by ureterocalicostomy on September 9, 1993. After clamping of the renal artery, the lowermost portion of the renal parenchyma was resected, and the lower calyx was sufficiently exposed. Adequate hemostasis of the cut surface was made, and the renal artery was then declamped. Many stones, measuring 20 mm or less, were removed through the lower calyx, and the lower calyx and the ureter were anastomosed. After operation, ESWL was additionally performed for residue stones. The IVP in July 1997 demonstrated the sufficiently patent anastomosed site without hydronephrosis or recurrence of nephrolithiasis. DISCUSSION: Anastomosis between the lower calyx and the ureter is an effective therapeutic method because it dose not interfere urine stream or small stone passage. However, it is not easy to make anastomosis in this site because the calyceal wall is very fragile. Several cases have been reported to have stenosis in the anastomosed site. We supposed that it is an excellent method for the treatment of refractory nephrolithiasis if the procedure is selected only for appropriate candidates.
Between January 1st, 1988 and May 31st, 1989, 667 patients (419 men, 248 women) with radioopaque, non cystinic and apparently idiopathic (lack of severe renal disease) renal stones were entered in a prospective study. The data obtained at entry enabled us to build up, retrospectively, a quantified presentation of the natural history of calcium nephrolithiasis. At the time the disease was discovered the patients' mean age was 40.4 years, and its presence had been known for 7.9 years on average in both sexes. The mean number of stones formed by the patients was 3.5. In 218 of the 277 patients who had only one stone the nephrolithiasis had been present for less than 3 years, as compared with at least 6 years in the 184/252 patients who had 3 stones or more; this suggests that in many of the patients studied the stones had rapidly become symptomatic. Women had a significantly (chi 2: P less than 10(-3)) more frequent history of urinary tract infection than men, and notably more frequent episodes of febrile infection (31.5 percent in women, 7.1 percent in men). A familial history of nephrolithiasis was found in 34.7 percent of women and 31 percent of men, but its presence had no influence on the number of stones formed or on the duration of the disease. On the other hand, the stones were discovered significantly earlier in men who has a familial history of nephrolithiasis (37.3 years) than in those who had no such history (42 years; P less than 10(-3)). These data will be used as baselines to a prospective evaluation of the course of nephrolithiasis in these patients.
BACKGROUND: five percent of consultations at the Emergency Room of Catholic University Hospital are due to nephrolithiasis. The causes of this high frequency remain unknown. AIM: to know the main metabolic and anatomic factors involved in the genesis of neprholithiasis. PATIENTS AND METHODS: forty one patients (31 male) were studied presenting with a renal colic were studied as soon as the acute episode subsided and without diet modifications. Fasting blood calcium and creatinine and 24 h urine calcium, uric acid, citrate, magnesium and pH were measured and an intravenous pyelogram was performed. Twenty one subjects without a history of nephrolithiasis were used as controls. RESULTS: Patients with nephrolithiasis did not differ from controls in urinary calcium (159 +/- 67 and 172 +/- 67 mg/24 h respectively), uricosuria (417 +/- 171 and 431 +/- 121 mg/24 h respectively) or urinary magnesium (55 +/- 19 and 62 +/- 21 mg/24 h respectively, whereas urinary citrate was lower (219 +/- 172 vs 319 +/- 179 mg/24 h in controls p < 0.05). All patients had normal renal functions, urinary acidification and intravenous pyelogram. Seven percent of patients with nephrolithiasis had hypercalciuria, 2.4% had hyperuricosuria. 68.3% had a low urinary citrate and 44.4% had low urinary magnesium. CONCLUSIONS: in this sample, there is a strong association of nephrolithiasis with low levels of crystallization inhibitors in special with urinary citrate, a crystallization inhibitor.
INTRODUCTION: The causes of nephrolithisis are multifactorial and have not yet been enough investigated [1]. Hypercalciuria is the most common cause of metabolic nephrolithiasis [2-4]. Close relationship between urinary calcium and urinary sodium has been a subject of reported observations in the past, showing that high urinary sodium is associated with high urinary calcium [5-7]. Hyperoxaluria, hyperuricosuria and cystinuria are also metabolic disorders that can lead to nephrolithiasis. Recent studies have indicated that urinary elimination of cystine is influenced by urinary sodium excretion. Based on these observations it has been hypothesised that patients with high urinary sodium excretion are at high risk of urinary stone disease. The purpose of the study was to investigate sodium excretion in a 24-hour urine and first morning urine collected from children with lithogenic metabolic abnormalities (hypercalciuria, hyperoxaluria, hyperuricosuria, cystinuria), both with nephrolithiasis and without it, in order to determine its significance in urinary calculi formation. PATIENTS AND METHODS: Urinary sodium excretion was investigated in 2 groups of children: patients with lithogenic metabolic abnormalities, but without urinary stone disease (L group) and patients with nephrolithiasis (C group). Both groups were divided into 2 subgroups: patients with hypercalciuria and without it. There were 22 patients in group L (mean age 11.97 +/- 4.13 years), of whom 17 formed a hypercalciuric subgroup and 5 formed a non-hypercalciuric subgroup (3 patients with hyperuricosuria and 2 patients with hyperoxaluria). Group C consisted of 21 patients with nephrolithiasis (mean age 12.67 +/- 3.44 years), of whom 6 formed a hypercalciuric subgroup and 15 formed a non-hypercalciuric group (2 patients with cystinuria and 13 patients without lithogenic metabolic abnormalities). Control group consisted of 42 healthy age-matched children. All subjects had a normal renal function. A detailed history and clinical examination were done, and ultrasonography was performed in all patients. A 24-hour urine, first morning urine and serum specimen were analysed for sodium, potassium, calcium, uric acid, urea and creatinine. Fractional excretion of sodium, as well as urinary sodium to creatinin ratio and urinary sodium to potassium ratio, were calculated from the findings. Sodium and potassium levels were determined by flame photometry, calcium was measured by atomic absorption technique (Beckman Atomic Spectrophotometer, Synchron CX-5 model, USA), uric acid by carbonate method and creatinine by Jaffe technique. Cystine and dibasic amino acids were quantified by ion chromatography. Urinary oxalate excretion was determined by enzyme spectrophotometry. Hypercalciuria was defined by 24-hour calcium excretion greater than 3.5 mg/kg per day and/or calcium to creatinine ratio greater than 0.20 [8]. Uric acid excretion was expressed as uric acid excretion factored for glomerular filtration, according to Stapleton's and Nash's formula [9]. Normal values were lower than 0.57 mg/dl of glomerular filtration rate in 24-hour samples. Mean values were statistically analyzed by Pearson's linear correlation and analysis of variance (ANOVA). RESULTS: Urinary sodium concentration values including urinary sodium to potassium ratios, are shown in Table 1. We found that urinary sodium excretion was significantly increased in patients of both L and C groups when compared with controls (p < 0.05). Further analysis of the subgroups showed that urinary sodium excretion was significantly higher only in patients with hypercalciuria of both L and C groups in comparison to controls (p < 0.05) (Table 2). A significant positive correlation was found between 24-hour urinary sodium to creatinine ratio and urinary calcium to creatinine ratio (r = 0.31; p < 0.001) (Graph 1), as well as between urinary sodium to potassium ratio in 24-hour and first morning urine (r = 0.69; p < 0.001) (Graph 2). (A
BACKGROUND: Because nephrolithiasis has been associated with obesity, an important risk factor for type 2 diabetes mellitus (DM), we tested the hypothesis that DM prevalence is increased in individuals who develop renal stones. METHODS: In an initial electronic analysis, prior diagnoses of DM, hypertension, and obesity were compared between all Olmsted County, MN, residents with a diagnosis code for nephrolithiasis between 1980 and 1999 and matched residents of similar age and sex (N = 3,561 case-control pairs). A random sample of 260 cases and corresponding controls was selected for detailed medical record review to confirm and characterize the stone event and obtain heights, weights, blood pressures, and glucose and cholesterol values. RESULTS: In the electronic analysis, unadjusted odds ratios (ORs) for DM (OR, 1.29; 95% confidence interval [CI], 1.09 to 1.53), obesity (OR, 1.15; 95% CI, 1.02 to 1.31), and hypertension (OR, 1.19; 95% CI, 1.04 to 1.35) were increased significantly for nephrolithiasis cases versus controls; DM remained significant after adjustment for age, sex, calendar year, hypertension, and obesity (OR, 1.22; 95% CI, 1.03 to 1.46). Detailed record review of a subset showed significant increases for cases versus controls for body mass index (OR, 1.05; 95% CI, 1.01 to -1.09) and hypertension (OR, 1.71; 95% CI, 1.17 to 2.59). Odds for DM were increased, but not significantly, in the subsample (OR, 1.44; 95% CI, 0.76 to 2.72). Among cases with stone analyses, those with uric acid stones (n = 10) had a greater percentage of DM compared with those with all other stone types (n = 112; 40% versus 9%; P = 0.02). CONCLUSION: Findings from this population-based study suggest that DM, obesity, and hypertension are associated with nephrolithiasis, and DM may be a factor in the development of uric acid stones.
In the years 1962--1975, at the Urological Department of the District Hospital in Warsaw, 1607 patients were operated on because of nephrolithiasis. In two cases coexistence of nephrolithiasis with renal tumour was demonstrated during operation. Physical and preoperative X-ray examinations suggested neither tumour nor metastatic foci in these two patients. The coexistence of nephrolithiasis and tumour of the kidney is a rarity (in our material 0.12%). Lumbotomy carried out because of nephrolithiasis makes possible a precise evaluation of the kidney condition and early discovery of tumour producing no clinical symptoms or X-ray changes.
Distal renal tubular acidosis (dRTA) is generally associated with hypercalciuria, hypocitraturia, and nephrolithiasis. Our intention was to study glycosaminoglycans (GAGS) and nephrocalcin (NC), two well-known crystal growth inhibitors, in a population with endemic dRTA and nephrolithiasis in northeast (NE) Thailand. We studied 13 patients, six with dRTA and seven with nephrolithiasis with normal or undefined acidification function. Six healthy adults living in the same area as the patients and another six from the Bangkok (BKK) area were used as controls. We measured urinary pH, ammonia, calcium, citrate, magnesium, oxalate, potassium, sodium and uric acid. GAGS were determined by an Alcian blue precipitation method and were qualitated by agarose gel electrophoresis after being isolated using 5% cetyltrimethylammonium bromide at pH 6.0. NC isoforms were isolated as previously described by Nakagawa et al. Citrate was higher in BKK controls ( p<0.04). There was a striking difference among GAGS from BKK when compared with other groups (103.85+/-10.70 vs. 23.52+/-8.11 for dRTA, 22.36+/-14.98 for kidney stone patients and 14.73+/-2.87 mg/ml in controls from the NE region, ( p<0.0001). dRTA and stone-forming patients excrete proportionally more (C+D) than (A+B) NC isoforms ( p<0.05). Also, their NC showed a 100-fold weaker binding capacity of calcium oxalate monohydrate crystals. The ratio of chondroitin sulfate/heparin sulfate in GAGS was approximately 9/1. In addition to the traditional risk factors for nephrolithiasis in dRTA, GAGS and NC might play an important role in the pathogenesis of stone formation in this population.
Nephrolithiasis is responsible for 1 in 1000 to 1 in 7600 pediatric hospital admissions annually throughout the United States. Seventy-five percent of children with nephrolithiasis have an identifiable predisposition to stone formation. This article reviews the different causes and disease states associated with nephrolithiasis in the pediatric population. The initial evaluation and the metabolic evaluation of children with nephrolithiasis are reviewed. Treatment modalities for the different stone types are also described.
PURPOSE: Nephrolithiasis in preterm infants rarely requires surgical management. When it persists despite conservative therapy, treatment options are not clearly defined. We report a single institutional experience with extracorporeal shock wave lithotripsy (ESWL)* for the treatment of these small infants. MATERIALS AND METHODS: We treated 8 infants (mean age 13 months) with a history of prematurity and 9 persistent stones with a Dornier HM3 lithotriptor between 1996 and 1999. Mean weight was 7,700 gm. Of the infants 7 had been treated with furosemide for bronchopulmonary dysplasia and 1 presented with multiple anatomical abnormalities. Gantry modification with a wooden platform and polystyrene foam positioning was used for lung and visceral protection. Ureteral stents were placed in 5 patients before ESWL. Renal ultrasonography was performed before, and 2 and a mean of 8 weeks after ESWL. Stone risk factors in our population were investigated through a multispecialty approach. RESULTS: Average stone burden was 47.9 mm.2. A total of 9 sessions of ESWL were required for complete fragmentation of the 9 renal stones. A mean total of 2,100 shocks at a mean 16.1 kV. were administered. One patient with bilateral stones was treated in 2 separate sessions after a 4-week interval. No repeat ESWL sessions or other surgical interventions were required in any patient. Renal ultrasonography demonstrated no post-ESWL morphological changes. Practices leading to a higher incidence of neonatal nephrolithiasis at our institution were also identified. CONCLUSIONS: ESWL is effective treatment for nephrolithiasis in small infants. Short-term safety has been established but continued long-term functional followup is essential. Multifactorial etiologies of nephrolithiasis must be identified and modified promptly in the care of preterm infants.
The formation of stones in the urinary tract stems from a wide range of underlying disorders. That clinicians look for the underlying causes for nephrolithiasis is imperative to direct management. There are many advances in genetics, pathophysiology, diagnostic imaging, medical treatment, medical prevention, and surgical intervention of nephrolithiasis. Here, I provide a brief general background and focus mainly on pathophysiology and medical treatment of kidney stones. Although important advances have been made in understanding nephrolithiasis from single gene defects, the understanding of polygenetic causes of kidney stones is still largely elusive. A substantial proportion of data that resulted in new methods of treatment and prevention, which can be empirical or definitive, has focused on urinary luminal chemical composition of the precipitating solutes. Manipulation of inhibitors and epithelial factors is important and needs further investigation. Advances in the management of nephrolithiasis depend on combined efforts of clinicians and scientists to understand the pathophysiology.
Indinavir sulfate has been reported to cause asymptomatic crystalluria and nephrolithiasis in patients with human immunodeficiency virus (HIV) infection. Patients taking indinavir may present with asymptomatic crystalluria, nephrolithiasis with frank renal colic and obstruction, flank pain in the absence of nephrolithiasis, and dysuria or urgency. Asymptomatic crystalluria has been described as benign. Discontinuation of the drug has not been recommended in the absence of nephrolithiasis. We report two HIV-positive patients receiving indinavir who developed acute interstitial nephritis with foreign body giant cell reaction on renal biopsies. Both patients had asymptomatic crystalluria, although crystals were associated with clumps of white blood cells (WBCs) on urinalysis in one patient. Both cases show that the inflammatory response was significant enough to lead to tubular injury and acute renal impairment. Our findings suggest that asymptomatic crystalluria attributable to indinavir may illicit an inflammatory response with acute renal insufficiency, warranting monitoring of renal function, especially in patients with crystalluria.
We performed a prospective study of patients with suspected ureteral colic to evaluate the test characteristics of bedside renal ultrasonography (US) performed by emergency physicians (EPs) for detecting hydronephrosis, and to evaluate how US can be used to predict the likelihood of nephrolithiasis. Thirteen EPs performed US, recorded the presence of hydronephrosis, and made an assessment of the likelihood of nephrolithiasis. All patients underwent i.v. pyelography (IVP) or unenhanced helical computed tomography (CT). There were 126 patients in the study: 84 underwent IVP; 42 underwent helical CT. Test characteristics of bedside US for detecting hydronephrosis were: sensitivity 72%, specificity 73%, positive predictive value (PPV) 85%, negative predictive value (NPV) 54%, accuracy 72%. The PPV and NPV for the ability of the EP to predict nephrolithiasis after performing US were 86% and 75%, respectively. We conclude that bedside US performed by EPs may be used to detect hydronephrosis and help predict the presence of nephrolithiasis.