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PubMed1983

Bilateral nephrolithiasis: simultaneous operative management.

A total of 14 patients with extensive bilateral nephrolithiasis underwent simultaneous bilateral lithotomy, in most instances through a single transabdominal incision. Anatrophic nephrolithotomy was performed on 25 kidneys, while 3 kidneys were approached in other ways without formal hypothermia and ischemia. There was no statistically significant change in the average preoperative and postoperative serum creatinine values (p greater than 0.1). There were residual stone fragments in 2 of the 28 kidneys (7 per cent) and stones recurred in 3 others (11 per cent) during the followup period (average 12 months). Of the 14 patients 10 (71 per cent) had infected urine preoperatively and 9 (64 per cent) have been free of infection postoperatively. There were no operative deaths and the average postoperative hospital stay was 17.6 days. We herein demonstrate that bilateral renal surgery for stone removal in 1 operative session can be performed safely with results comparable to those of unilateral staged procedures using other approaches. The advantages of this type of surgical management are discussed.

Adult↗

PubMed1980

Successive appearance of carcinoma, tuberculosis and nephrolithiasis in a renal allograft.

A small renal cell carcinoma was transplanted inadvertently with a kidney from a living donor and was treated with partial nephrectomy. Secondarily, tuberculosis of the renal allograft appeared, which was followed by nephrolithiasis. The kidney was left in place, immunosuppressive treatment was continued and renal function is normal more than 8 years after transplantation, with no sign of the cancer progressing or reactivation of the tuberculosis.

Adenocarcinoma↗

PubMed1978

Effects of magnesium oxide on the crystallization of calcium salts in urine in patients with recurrent nephrolithiasis.

The effect of oral administration of magnesium oxide on the crystallization in urine of calcium oxalate and brushite was determined in 4 cases of recurrent calcium nephrolithiasis. Each patient was evaluated while on a constant metabolic diet before, during and after therapy with magnesium (1,000 mg. magnesium as magnesium oxide per day). During magnesium therapy urinary hydrogen ion concentration increased by approximately 0.5 unit in all 4 patients and urinary calcium increased about 50 mg. per day in 2. Urinary oxalate decreased significantly in 1 patient and urinary phosphorus was reduced in 2. The urinary activity product ratio of brushite (state of saturation) increased, owing largely to the rise in urinary hydrogen ion concentration but that of calcium oxalate was not changed significantly by magnesium treatment. Although urinary magnesium increased significantly there was no significant change in the urinary formation product ratio (limit of metastability) or the rate of crystal growth of brushite or calcium oxalate. Thus, no beneficial effect of magnesium therapy could be demonstrated in this short-term study.

Administration, Oral↗

PubMed1975

Pediatric nephrolithiasis.

The management of 78 children with upper urinary calculi is described. Boys outnumbered girls by a ratio of 2 to 1. Two-thirds of the patients had identifiable metabolic causes, while the remaining third had infected renal lithiasis. In this latter group, all patients had had multiple urologic procedures, urinary infection, and stasis with diversionary and indwelling drainage devices. Contrary to earlier views, idiopathic renal lithiasis with or without hypercalciuria was the most common metabolic form of nephrolithiasis in children. Sixty-seven patients (86 per cent) were followed for an average of 7 1/2 years. With appropriate therapy, stone disease became inactive in 70 per cent of the children. The remaining 30 per cent continued with active disease--5 died of renal failure and 1 has received a renal allograft. Stone formation may be regarded as a solitary complication or one of several manifestations of a large number of underlying disorders. Along with a thorough search for etiologic factors there must be an equally aggressive therapeutic effort. Because the disease is ofter sporadic, careful long-term followup of the patients with active as well as those with inactive stone disease is mandatory.

Acidosis, Renal Tubular↗

PubMed2003

Role of urinary inhibitors of crystallization in uric acid nephrolithiasis: Dalmatian dog model.

OBJECTIVES: To study the role of urinary inhibitors on crystallization-nephrocalcin, Tamm-Horsfall protein (THP), and glycosaminoglycans (GAGs)-in hyperuricosuric nephrolithiasis using Dalmatian dogs, a breed well-known for high levels of uric acid excretion, in an in vivo model. METHODS: Urine samples were collected from 10 stone-forming Dalmatian dogs and from 5 age-matched Dalmatians without kidney stones. Purine derivatives present in urine were studied by high-performance liquid chromatography. THP, GAGs, and nephrocalcin were isolated and measured. RESULTS: As expected, the Dalmatians excreted a large amount of uric acid in urine, but without differences between the two groups (0.42 +/- 0.08 mg/mg creatinine versus 0.48 +/- 0.11 mg/mg creatinine for stone-forming and healthy Dalmatians, respectively, P = 0.64). No other metabolites were derived from purine in their urine. Stone-forming Dalmatians showed significantly lower urinary excretion of THP than did normal Dalmatians (0.09 +/- 0.03 mg/mg creatinine versus 0.21 +/- 0.03 mg/mg creatinine, P <0.03). The urinary excretion of GAGs was lower in the stone-forming Dalmatians, although the difference was not statistically significant. Inhibition of calcium oxalate monohydrate crystal growth caused by nephrocalcin isoforms from healthy and stone-forming dogs were in the same order of approximately 10(-7) M, as calculated from a Langmuir isotherm type plot. CONCLUSIONS: The urinary excretion of THP and GAGs was decreased in stone-forming Dalmatians compared with healthy ones. Our results support the suitability of Dalmatian dogs as an in vivo model to investigate the interrelationship of urine inhibitors of crystallization and hyperuricosuria.

Animals↗

PubMed2003

Urinary glycosaminoglycans as risk factors for uric acid nephrolithiasis: case control study in a Sardinian genetic isolate.

OBJECTIVES: To assess the clinical association between glycosaminoglycan (GAG) excretion and uric acid (UA) nephrolithiasis by measuring urinary GAG levels in a case-control study conducted in a Sardinian genetic isolate. Inhibitors of crystallization such as GAGs seem to be involved in kidney stone formation. METHODS: Overnight (12-hour) urinary excretion of GAGs, calcium, oxalate, and UA were measured in urine samples from 60 patients who had formed at least one urinary stone (UA or mixed) and 52 healthy controls. The total GAG concentration was measured by a dye-binding assay, and the values were normalized against creatinine to obtain values in micrograms of GAG per milligram creatinine. Statistical analysis was performed using t tests and logistic regression analysis. RESULTS: No significant difference was found between the two groups with respect to calcium and oxalate concentrations. Nonetheless, stone formers had significantly lower levels of GAGs (29.5 +/- 2.2 versus 36.4 +/- 3.9 microg/mg creatinine, P = 0.003) and greater levels of UA (385.11 +/- 38.2 versus 298.43 +/- 31.4 mg/12 hr, P = 0.0010) than did the normal controls. CONCLUSIONS: We report that the lower excretion of GAGs in stone formers could impair their inhibitory activity on UA stone formation, and, as a consequence, it may represent a risk factor for this form of urolithiasis.

Case-Control Studies↗

PubMed1996

Nephrolithiasis due to primary hyperparathyroidism and enteric hyperoxaluria: a case report.

Enteric hyperoxaluria and primary hyperparathyroidism have been associated with the development of nephrolithiasis. We report a case involving a patient who had hyperparathyroidism due to a parathyroid adenoma and enteric hyperoxaluria resulting from a small bowel bypass and who had severe stone-related complications. This combination of stone-generating factors has heretofore not been reported. The pathophysiology of these entities is discussed.

Adult↗

PubMed2000

When and how to evaluate a patient with nephrolithiasis.

Nephrolithiasis is a common disorder that afflicts up to 12% of the population and continues to be a significant cause of patient injury. Evaluation of these patients should include the assessment of their comorbidities and underlying medical conditions. Patients who form stones can undergo a streamlined evaluation. A cause can be found in more than 90% of these patients. With medical treatment, stone-recurrence rates can be decreased by 85% for calcium oxalate stone formation, which affects a large proportion of patients. Introduction of nonspecific medical therapy in uncomplicated calcium stone disease may improve the quality of life for these patients and allow utilization a simple diagnostic protocol. This is in contrast to the previous recommendations of disease-specific therapy. Because patients without complications represent the majority of those who form stones, a simplified approach greatly reduces the cost of evaluation and treatment. Underlying medical conditions, however, require disease-specific therapy. The protocol represented here should aid physicians and patients in the approach to management of stone disease. The fasting calcium-load test is not required, and the entire evaluation can be performed in an ambulatory setting in two visits. Two 24-hour urine samples should be obtained on a random and restricted diet. Patients who form calcium stones can be subdivided into those who form hypercalciuric and normocalciuric stones. Patients who form normocalciuric stones are treated with conservative measures (increased fluid intake) and potassium and magnesium citrate. Patients who form hypercalciuric stones are treated with a combination of thiazides and potassium and magnesium citrate.

Acidosis, Renal Tubular↗

PubMed1997

Uric acid-related nephrolithiasis.

Abnormalities in uric acid metabolism are associated with uric acid and calcium oxalate urolithiasis. Clinical stone formation depends on multiple identifiable risk factors that affect uric acid and calcium oxalate solubility. The understanding of urinary pH is critical to direct appropriate treatment of uric acid-related nephrolithiasis. Understanding uric acid metabolism and the pathophysiology of uric acid and calcium oxalate stone formation leads to a rational treatment approach to uric acid and hyperuricosuric calcium oxalate stone disease.

Calcium↗

PubMed1987

Nephrolithiasis in pregnancy.

Despite anatomic and physiologic changes that predispose to stone formation, nephrolithiasis in pregnancy remains an uncommon occurrence. Stones occur more frequently in multiparas, during the later stages of gestation, and without a difference in laterality. Correct diagnosis can be confusing. Ultrasound has become a primary diagnostic tool and limited excretory urograms are only recommended for complicated cases. Conservative management can result in spontaneous passage of most stones. When necessary, cystoscopy or surgery can be done safely. Preexisting stone disease is associated with an increased incidence of urinary tract infections in pregnancy. Renal colic often precipitates premature labor. Most drugs used to treat stone disease are contraindicated in gestation. Increased quantities of known inhibitors of stone formation are present in gestation and may explain why the incidence of stones is not increased in this hypercalciuric state.

Colic↗

PubMed1997

Acute renal failure due to indinavir crystalluria and nephrolithiasis: report of two cases.

Two patients with oliguric acute renal failure (ARF) attributed to crystalluria and nephrolithiasis with obstructive uropathy caused by the human immunodeficiency virus protease inhibitor indinavir are described. In both patients, ARF resolved with administration of intravenous fluids. One patient required urologic intervention to relieve bilateral ureteral obstruction.

Acute Kidney Injury↗

PubMed2002

Risk of calcium oxalate nephrolithiasis in postmenopausal women supplemented with calcium or combined calcium and estrogen.

BACKGROUND: Recent studies showed that postmenopausal women lost less bone mass when supplemented with calcium or estrogen therapy. However, the safety of the treatments in terms of the risk of calcium oxalate stone formation is unknown. We therefore conducted this study to determine the alteration in calcium oxalate supersaturation after calcium supplement or after combined calcium and estrogen therapy in postmenopausal osteoporotic women. METHODS: Fifty-six postmenopausal women were enrolled in this study. All subjects were more than 10 years postmenopausal with vertebral or femoral osteoporosis by bone mineral density criteria. They were randomly allocated to receive either 625 mg of calcium carbonate (250 mg of elemental calcium) at the end of a meal three times a day (group A, n=26) or calcium carbonate in the same manner plus 0.625 mg/day of conjugated equine estrogen and 5 mg medrogestone acetate from day 1-12 each month (group B, n=30). The age (mean +/- S.E.M.) was 66.3 +/- 1.2 and 65.1 +/- 1.1 years, weight 54.1 +/- 1.2 and 55.3 +/- 2.1 kg, in group A and group B, respectively. Urine specimens (24-h) were collected at baseline and 3 months after treatment for the determination of calcium oxalate saturation by using Tiselius's index (AP(CaOx)) and calcium/citrate ratio. RESULTS: After 3 months of treatment, there was no significant alteration from baseline for urinary excretion of calcium, citrate and oxalate. Urinary phosphate excretion was significantly reduced (6.3 +/- 0.7 vs. 5.1 +/- 0.7 mmol/day for group A and 8.2 +/- 0.9 vs. 5.8 +/- 0.7 mmol/day for group B, P<0.05), whereas net alkaline absorption was significantly elevated (10.1 +/- 3.6 vs. 20.1 +/- 4.4 meq/day for group A and 4.8 +/- 3.2 vs. 19.9 +/- 3.6 meq/day for group B, P<0.05). Calcium/citrate ratio and AP(CaOx) determined at baseline were not different from the corresponding values after treatment in both groups; calcium/citrate: 10.1 +/- 3.1 vs. 10.1 +/- 2.5 for group A and 9.3 +/- 1.8 vs. 11.9 +/- 2.5 for group B and AP(CaOx): 1.1 +/- 0.1 vs. 1.3 +/- 0.2 for group A and 1.2 +/- 0.2 vs. 1.1 +/- 0.1 for group B. There were eight and nine patients with high AP(CaOx), or >2, at baseline and after treatment, respectively. CONCLUSIONS: Calcium supplement with a meal or combined calcium supplement and estrogen therapy is not associated with a significant increased risk of calcium oxalate stone formation in the majority of postmenopausal osteoporotic patients. Determination of urinary saturation for calcium oxalate after calcium and estrogen supplements, especially at the initial phase of treatment, may be helpful in the avoidance of nephrolithiasis.

Aged↗

PubMed2001

Nephrolithiasis.

This article covers the diagnosis and management of renal colic. New imaging modalities will be reviewed using evidence-based medicine. The disposition of the patient with renal colic will be addressed. Additionally, special groups with nephrolithiasis will be discussed.

Adolescent↗

PubMed2002

Pathogenesis of hypercalciuric nephrolithiasis.

The major contribution of hypercalciuria in raising urinary state of saturation with respect to calcium salts and subsequent risk of nephrolithiasis is appreciated. Derangements in the physiological mechanisms that regulate calcium homeostasis and contribute to hypercalciuria have also been identified. New avenues of research are beginning to explore the specific defects that may contribute to hypercalciuria. From such studies, an understanding of the role of certain dietary excesses as contributors to the development of hypercalciuria and, in some cases, attendant bone loss, is beginning. The contribution of genetics to hypercalciuria has provided a powerful means of identifying genes that contribute to the hypercalciuric phenotype in a number of hypercalciuric conditions. Such studies have disclosed that hypercalciuria is probably polygenic in nature and will require a concerted effort to better understand the defects while attempting to develop gene-specific countermeasures.

Calcium↗

PubMed2002

Hyperoxaluric calcium nephrolithiasis.

Hyperoxaluria leads to increased calcium oxalate supersaturation and calcium oxalate stone formation. Excess oxalate can arise from endogenous overproduction as in primary hyperoxaluria or from dietary sources. In the last 15 years great strides have been made in the diagnosis and treatment of primary hyperoxaluria. However options still seem limited in treating the mild hyperoxaluria found in many stone formers. Inadequate knowledge of food oxalate content, the effect of dietary oxalate precursors on oxalate excretion, and the factors affecting handling of oxalate by the intestine prevent development of rational therapies for treatment of hyperoxaluria. Recent studies of oxalate degrading bacteria and renewed interest in the role of diet calcium in oxalate absorption may lead to better therapeutic strategies for hyperoxaluric calcium nephrolithiasis.

Adolescent↗

PubMed1994

Nephrolithiasis in pregnancy.

Although the anatomical and physiological changes of normal pregnancy may predispose to kidney stone formation, it remains an uncommon occurrence. Correct diagnosis is often difficult. Ultrasonography has become the primary radiological diagnostic tool, with a limited excretory urogram only necessary in complicated cases. Nephrolithiasis during pregnancy occurs more frequently during the later stages of gestation, in multiparas, and without a difference in laterality. Conservative management with bed rest, hydration and analgesia can result in spontaneous passage of most stones in gravidas. Past experience of several groups suggests that cystoscopy and/or surgery can usually be done safely when absolutely necessary. Pre-existing stone disease can increase the incidence of maternal urinary tract infections by 10-20%. The most common obstetric complications of stones during gestation is premature labour induced by renal colic. Most drugs normally used to treat stone disease are contraindicated in gestation. Known inhibitors of stone formation are present in gestation and may partially explain why the incidence of stones is not increased in this hypercalciuric state.

Adult↗

PubMed1987

Nephrolithiasis and gestation.

Although both anatomical and physiological changes in pregnancy may predispose to kidney stone formation, it still remains an uncommon occurrence. Correct diagnosis is often difficult. Ultrasound has become the primary diagnostic tool, and a limited study excretory urogram is only necessary for complicated cases. Nephrolithiasis during pregnancy occurs more frequently during the later stages of gestation in multiparas, and without a difference in laterality. Conservative management with bed rest, hydration and analgesia can result in spontaneous passage of the majority of stones in gravidas. Past experience indicates that cystoscopy and/or surgery can usually be done safely when absolutely necessary. Pre-existing stone disease can increase the incidence of maternal urinary tract infections by 10-20%. The most common obstetric complication of stones during gestation is the precipitation of premature labour by renal colic. Unfortunately, most drugs used to treat stone disease are contraindicated in gestation. Experimental evidence suggests that known inhibitors of stone formation are present in gestation, and may help to explain why the incidence of stones is not increased in this particularly hypercalciuric state.

Female↗

PubMed1982

Metolazone therapy of active calcium nephrolithiasis.

Metolazone, a nonthiazide diuretic with the hypocalciuric effect of the thiazides, was evaluated in patients with idiopathic calcium nephrolithiasis. During the mean 3-yr treatment period, there was a 77% decrease in stone incidence in 38 male patients (from 2.10 to 0.49 stones/patient/year). Urine calcium decreased 51% (from 231 +/- 19 to 114 +/- 7 mg/24 hr after 13 mo therapy). The treatment response was the same when these patients were divided into normocalciuric (n = 23), borderline hypercalciuric (n = 10), and hypercalciuric groups (n = 5). In six other patients with high sodium intake there was no decrease in urine calcium on stone formers regardless of the initial level of urine calcium excretion. High sodium intake may blunt and low intake potentiate the hypocalciuric effect of metolazone.

Calcium↗