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PubMed1997

Clinical and biochemical presentation of primary hyperparathyroidism in Kansai district of Japan.

Although the number of patients with primary hyperparathyroidism (pHPT) has increased since biochemical screening came to be widely employed, few data are available concerning the clinical analysis of Japanese patients. We therefore tried to determine the recent clinical and biochemical state of Japanese patients with pHPT. Clinical and biochemical data were analyzed in a series of 103 pHPT patients who had been hospitalized in Kobe University Hospital during a 17 year period from 1979 to 1995. The data were obtained from the hospital records and additionally from information through questionnaires performed in 1995. Patients were 29 males and 74 females. The average ages at diagnosis were 53.4 +/- 16.0 (SD) year-old and 53.9 +/- 15.2 year-old, respectively. The major clinical symptoms were nephrolithiasis (35.9%), thirst/polyuria (33.0%), easy fatigability (20.4%) and back pain/lumbago (16.5%), but 19.4% of the patients were asymptomatic. Out of 87 cases who received parathyroidectomy, 10 (11.5%) were diagnosed with parathyroid carcinoma. Age- and sex-corrected bone mineral density (BMD) of the radius was significantly lower in the group with back pain/lumbago than in the group without the symptom. Similarly, radial BMD was lower in the group with a high serum alkaline phosphatase value. Patients with nephrolithiasis had a lower urinary calcium/creatinine ratio (UCa/ UCr; 0.305 +/- 0.188 mg/mg) than the patients without nephrolithiasis (0.400 +/- 0.160 mg/mg). This inconsistent result suggests that some important factors except urinary calcium would contribute to urinary stone formation in pHPT. Our data mostly agreed with previous reports on a Caucasian population except for a relatively high prevalence of parathyroid carcinoma, but the negative correlation between nephrolithiasis and urinary calcium was not easily explicable. This finding should be confirmed by analyzing a larger number of cases.

Adolescent↗
PubMed2001

ClC-5 chloride channel and kidney stones: what is the link?

Nephrolithiasis is one of the most common diseases in the Western world. The disease manifests itself with intensive pain, sporadic infections, and, sometimes, renal failure. The symptoms are due to the appearance of urinary stones (calculi) which are formed mainly by calcium salts. These calcium salts precipitate in the renal papillae and/or within the collecting ducts. Inherited forms of nephrolithiasis related to chromosome X (X-linked hypercalciuric nephrolithiasis or XLN) have been recently described. Hypercalciuria, nephrocalcinosis, and male predominance are the major characteristics of these diseases. The gene responsible for the XLN forms of kidney stones was cloned and characterized as a chloride channel called ClC-5. The ClC-5 chloride channel belongs to a superfamily of voltage-gated chloride channels, whose physiological roles are not completely understood. The objective of the present review is to identify recent advances in the molecular pathology of nephrolithiasis, with emphasis on XLN. We also try to establish a link between a chloride channel like ClC-5, hypercalciuria, failure in urine acidification and protein endocytosis, which could explain the symptoms exhibited by XLN patients.

Animals↗
PubMed2000

[Hypocitraturia in children with urolithiasis].

Inhibitors of crystallization process play an important role in renal-stone forming patients. One of well-known inhibitor is citrate. The aim of the study was to define the type of metabolic abnormality in children with nephrolithiasis and the role of urinary citrate excretion. 52 children with nephrolithiasis were examined. Hypocitraturia was observed in 42.3% of patients, most frequently in children with hypercalciuria, hyperoxaluria, and hyperoxaluria with hyperuricosuria. Low urinary citrate excretion found in patients with nephrolithiasis may play an important role in the pathogenesis of the disease. Urinary citrate excretion should be examined in patients with nephrolithiasis.

Adolescent↗
PubMedDate not supplied

Medical prevention and treatment of urinary stones.

Despite revolutionary developments in minimally invasive methods for the removal of stones in the last 15 years, the medical prevention of urinary stones remains very rewarding, due to the continual increase in the prevalence of nephrolithiasis in western countries, the high recurrence rate of the disease, its complications, discomfort and the costs of lithotripsy. Medical prevention is highly effective (50-95% efficacy in different series) and cost-convenient; its basic elements are appropriate metabolic evaluation, adequate hydration, "common sense" diet, and, in selected cases, drugs of proven efficacy. Clinical-metabolic evaluation should aim at the recognition of specific types of nephrolithiasis, and sort out secondary and/or remediable cases, define urinary risk factors, assess patients' compliance and the side effects of any therapy during follow-up. Hydration has proved effective in clinical trials and population-based observational studies; "fluids" may consist of water (any kind), coffee (caffeinated or decaffeinated), tea, beer and wine; grapefruit juice appears to have an unexplained ill effect. Despite the lack of clinical demonstration that dietary manipulations reduce the recurrences of stones, biochemical and epidemiological data suggest that high sodium, animal protein and sucrose intake increase the risk. Undue reductions in Ca intake also appear to be detrimental both for stone recurrences and bone mineralisation: "adequate" Ca intake (800-1000 mg/day) should be encouraged, but only in food since supplemental Ca, as drugs, appears to increase the risk of stones. Effective drugs are available for cystine, uric acid, infected stones and several secondary causes of Ca nephrolithiasis; in "idiopathic" Ca nephrolithiasis, thiazides, allopurinol, K and K-Mg citrate and possibly neutral K phosphate have been shown to be effective, at least in specific metabolic contexts.

Beverages↗
PubMed2002

Primary hyperparathyroidism and the kidney: biochemical and clinical spectrum.

Primary hyperparathyroidism manifests biochemically as a disturbance in serum calcium homeostasis. The central organ setting serum calcium level is the kidney. It not only has the highest rate of active calcium transport, but the kidney also modulates serum calcium homeostasis by virtue of its endocrine role in 1,25-hydroxyvitamin D secretion. Receptors for PTH are widely expressed throughout the renal tubule and are involved in both calcium transport and endocrine function. Biochemical manifestations of primary hyperparathyroidism by the kidney include increased tubular reabsorption of calcium, decreased reabsorption of phosphate and bicarbonate, and hypercalciuria. A reduction in glomerular filtration may occur in some patients with primary hyperparathyroidism, which perturbs the diagnostic relationships among biochemical variables and induces further increases in PTH secretion. Parathyroidectomy rapidly restores the biochemical abnormalities to normal apart from chronic reduced glomerular filtration. Clinical manifestations are nephrolithiasis, which is common, and nephrocalcinosis, which is uncommon. Nephrocalcinosis may occur with or without nephrolithiasis. Risk factors for nephrolithiasis are oversaturation of urine with calcium phosphate and with calcium oxalate. Risk factors for nephrocalcinosis are not clearly defined. Parathyroidectomy greatly reduces the incidence of nephrolithiasis but has little effect on nephrocalcinosis.

Bicarbonates↗
PubMed2004

[Metabolic evaluation of recurrent idiopathic calcium stone disease in Portugal].

BACKGROUND: Idiopathic calcium stone disease is the most frequent type of nephrolithiasis in industrialised countries. Several metabolic, environmental and genetic factors have described and may be involved in its pathogenesis. This study was designed to evaluate the factors that contribute to idiopathic calcium stone disease in Portugal. METHODS: To characterise the Portuguese population with idiopathic recurrent calcium stone disease, a population of 87 consecutive idiopathic recurrent calcium stone formers (IRCSF) was evaluated over a 5-year period. The results were compared with a control group of 45 healthy subjects (HS) from the same population, with similar age and gender distribution. RESULTS: No difference was observed in the distribution of affected individual according to gender (47 females and 40 males). A familial history of nephrolithiasis was present in 35.6%. Significantly higher urinary calcium and lower urinary citrate were observed in IRCSF group when compared with HS group. Individual analysis revealed urinary abnormalities in 78 of 87 IRCSF (89.7%). Hyperoxaluria was the most frequent abnormality, observed in 40.2% of the patients, hyperuricosuria in 33.3%, hypercalciuria in 24.1%, hypocitraturia in 23.0%, low urine volume in 19.5% and hypomagnesiuria in 8%. No difference was observed in the distribution of urinary risk factors according to gender or presence of familial antecedents of nephrolithiasis. A positive correlation was observed between urinary sodium and calcium in hypercalciuric patients. CONCLUSIONS: Among the studied population, idiopathic calcium nephrolithiasis affected both genders equally. Metabolic evaluation permits the identification of urine abnormalities in most of these patients. Hyperoxaluria, hypercalciuria, hypocitraturia and hyperuricosuria appeared as important pathogenic factors in IRCSF. Urine volume was not different between groups. Dietary factors may be involved in the observed urine abnormalities and need to be further evaluated.

Adult↗
PubMedDate not supplied

[Pathogenesis of renal calculi].

The prevalence of nephrolithiasis (12% of the population) is directly related to environmental risk factors including nutrition. Correlations have been demonstrated between activity of renal stone disease and excessive protein intake or low fiber diets, and cause-and-effect relationships have been suggested between prevalence of the disease and low urine volume due to underhydration. Indeed eating too much meat and drinking too little can expose certain subjects, but not all, to nephrolithiasis. Why? Populations at risk include subjects with medullary sponge kidneys who represent 10% of the patients with idiopathic calcium nephrolithiasis and those with mild metabolic hyperoxaluria who cannot activate pyridoxin to 5' pyridoxal phosphate. Defective intestinal absorption of citrate and modifications in protein structures which inhibit urinary crystallization have also been observed. Clearly, many apparently normal subjects are overly susceptible to nephrolithiasis and the "explosion" would appear to be programmed if they are exposed to additional risk factors. Thus our theory of the powder keg and the tinderbox.

Cholelithiasis↗
PubMedDate not supplied

[Functional evaluation in patients with kidney calculi].

Nephrolithiasis is a common disorder and a significant problem because of incidence, recurrence and severe consequences. Stone disease is a surgical as well as a medical problem. Major progress has been made recently in understanding the pathophysiological disturbances responsible for stone formation as well as in the techniques of stone removal. The introduction of extracorporeal shock wave lithotripsy has considerably reduced the need for surgery. Improvements in methods of kidney stone removal have not diminished the need for the application of an effective prophylactic program. The internist should take a complete history of stone events (number, composition, location and outcome of stone event), family history of stones, dietary habits (focusing on the consumption of animal protein, salt and dairy products), medications and physical examination. Radiopaque stones should be documented by plane X-ray films. Ultrasonography should be used to image calculi that are nonopaque, and to easily distinguish them from masses such as tumour or blood clot. Computed tomography is also an excellent method for imaging nonopaque renal calculi but higher cost and radiation exposure are disadvantages [2]. Crystallographic analysis is the essential diagnostic procedure. If available, previous stones should also be examined. "In stone disease, everything is measurement. What the laboratory cannot tell you, you will not know; what it tells you in error, you will not correct by using your instincts, your medical experience, or your art [3]". Reliable diagnostic protocols are available for the identification of different causes of stones. The complexity of protocols depend on the severity of nephrolithiasis. Patients with a single stone episode undergo simple protocol, and extensive detailed protocol is used for patients with recurrent stone disease, or patients at increased risk. Simple protocol, besides the already mentioned history of stone events, radiographic investigation and crystallographic analysis, includes serum urea, creatinine, uric acid, sodium, calcium, phosphorus and protein levels, urinary pH and volume, urine samples for culture and urinary calcium, uric acid, oxalate and citrate. Extensive metabolic evaluation includes simple protocol, determination of serum levels of alkaline phosphatase, parathyroid hormone, thyroxin, magnesium. A 24-h collection of urine specimen is analysed for urea, creatinine, uric acid, calcium, phosphate, sodium, magnesium, oxalate and citrate. Extensive protocol includes specialized evaluation tests [5]. Urinary acidification test is important for detecting distal renal tubular acidosis. Two 24-h urine specimens are collected while the patient is on the regular diet. The patient is then placed on a restricted diet (400 mg of calcium and 100 mEq of sodium) for a week, and another 24-h urine sample is collected. After that fasting and calcium load tests are performed (Sheme 1). Fasting urinary calcium is used to detect renal calcium leak, and calciuric response to oral calcium load provides an indirect measure of intestinal calcium absorption. Diagnostic criteria for major forms of stone disease [8] are presented in Table 1. There are some still unsolved questions: does time after passage of stones or urological intervention influence the frequency of urine abnormalities that can be detected; are there differences in 24-h urine composition between weekdays and weekends: what is the prevalence of the most important urinary risk factors of recurrent idiopathic calcium nephrolithiasis: do male patients differ from females with respect to urinary risk factors or recurrent idiopathic calcium nephrolithiasis? [7].

Humans↗
PubMed2006

Acute renal failure from xanthine nephropathy during management of acute leukemia.

Tumor lysis syndrome is a potentially life-threatening complication of induction chemotherapy for treatment of lymphoproliferative malignancies. Serious complications of tumor lysis syndrome are rare with the preemptive use of allopurinol, rasburicase, and urine alkalinization. We report a case of oliguric acute renal failure due to bilateral xanthine nephropathy in an 11-year-old girl as a complication of tumor lysis syndrome during the treatment of T-cell acute lymphoblastic leukemia. Xanthine nephrolithiasis results from the inhibition of uric acid synthesis via allopurinol which increases plasma and urinary xanthine and hypoxanthine levels. Reports of xanthine nephrolithiasis as a cause of tumor lysis syndrome are rare in the absence of defects in the hypoxanthine-guanine phosphoribosyl transferase (HGPRT) enzyme. Xanthine nephropathy should be considered in patients who develop acute renal failure following aggressive chemotherapy with appropriate tumor lysis syndrome prophylaxis. Urine measurements for xanthine could aid in the diagnosis of patients with nephrolithiasis complicating tumor lysis syndrome. Allopurinal dosage should be reduced or discontinued if xanthine nephropathy is suspected.

Acute Kidney Injury↗
PubMed1988

Biochemical changes before and during oral calcium tolerance test in calcium stone formers.

116 normocalcemic and 8 primary hyperparathyroid (PHPT) patients with calcium (Ca) nephrolithiasis and 10 normal controls underwent 1 g of oral Ca tolerance test following 4 days of Ca restricted diet (400 mg/day). On the basis of urinary Ca/creatinine (Cr) ratio obtained by the test, the 116 patients with normocalcemic nephrolithiasis were divided into 3 groups (normocalciuric nephrolithiasis; NN, absorptive hypercalciuria; AH, renal hypercalciuria; RH) according to our criteria which were slightly modified from Pak et al. Changes in urinary Ca/Cr ratio, and those in serum Ca and phosphorus (P), tubular maximum reabsorption of phosphate/glomerular filtration rate (TmPO4/GFR), nephrogenous adenosine 3',5'-monophosphate (NcAMP) and plasma immunoreactive parathyroid hormone (iPTH) were determined. As a result, the 116 patients were divided into 82NN, 13AH and 21RH. In general, a rise in serum Ca and fall in NcAMP were seen first, followed by rises in urinary Ca/Cr ratio, serum P and TmPO4/GFR although the changes were small. The group PHPT showed abnormality in the changes of TmPO4/GFR, NcAMP and plasma iPTH. The former one decreased constantly during the test and the latter two did not fall to within the normal range, suggesting parathyroid autonomy or abnormal suppressibility. Regarding the normal controls, all the changes were smallest among the 5 groups and clear parathyroid suppression was not observed while it was seen in the groups NN, AH and RH. In conclusion, oral Ca tolerance test is useful not only to separate NN, AH and RH, but also for the diagnosis of PHPT by demonstrating parathyroid autonomy or abnormal suppressibility assessed by NcAMP and/or TmPO4/GFR.

Administration, Oral↗
PubMed2003

Identification of a novel splice site mutation of CLCN5 gene and characterization of a new alternative 5' UTR end of ClC-5 mRNA in human renal tissue and leukocytes.

Mutations in the CLCN5 gene have been detected in Dent's disease and its phenotypic variants (X-linked recessive nephrolithiasis, X-linked recessive hypophosphatemic rickets, and idiopathic low-molecular-weight proteinuria of Japanese children). Dent's disease is a tubular disorder characterized by low-molecular-weight proteinuria, and nephrolithiasis associated with nephrocalcinosis and hypercalciuria. ClC-5 is the first chloride channel for which a definitive role in the trafficking and acidification-dependent recycling of apical membrane proteins has been established. In the course of CLCN5 SSCP analysis in patients with hypercalciuric nephrolithiasis, we detected a novel mutation at intron 2 of the CLCN5 gene, a T-to-G substitution, located 17 bp upstream of the AG acceptor site. To determine the effect of IVS2-17 T>G mutation on the correct splicing of intron 2, we studied ClC-5 transcripts in a patient's peripheral blood leukocytes by means of quantitative comparative RT/PCR, and found a new ClC-5 5' UTR isoform characterized by the untranslated exon 1b and by retention of intron 1b. This new isoform--isoform B1--was not correlated with mutation since it was detected also in control leukocytes and in renal tissues of kidney donors, thus confirming its physiological role. By RACE analysis we determined the putative transcriptional start site which is located at intron 1a, 251 nt upstream of the first nucleotide of the untranslated exon 1b. ORF analysis revealed that intron 1b retention in isoform B1 stabilizes the initiation of translation to the AGT at position 297 of the ClC-5 cDNA coding region.

5' Untranslated Regions↗
PubMed2001

Papillary necrosis associated with the HIV protease inhibitor indinavir.

The HIV protease inhibitor indinavir may cause nephrolithiasis and interstitial nephritis. The renal consequences of indinavir-associated nephrotoxicity are uncertain. We report a case of papillary necrosis in a patient treated with indinavir. An asymptomatic HIV-infected woman experienced right-sided renal colicky pain during treatment with indinavir. She passed a non-solid stone and continued indinavir treatment. Intravenous pyelogram performed 20 months later following an episode of left-sided colicky pain showed right-sided papillary necrosis. Indinavir-associated nephrolithiasis and chronic interstitial nephritis were the only possible causes identified in this patient. Physicians should be aware that indinavir nephrolithiasis may cause papillary necrosis.

Adult↗
PubMed1983

Immunopathogenesis of chronic pyelonephritis.

Immunopathologic responses to urinary Tamm-Horsfall protein in the development of chronic pyelonephritis were examined by four different approaches. First, in a rabbit model, tubulointerstitial nephritis developed in 64 of 102 rabbits injected intravenously with urine or rabbit Tamm-Horsfall protein as compared with only one of 17 rabbits in two control groups. Circulating cytotoxic lymphocytes plus immunoglobulin G (IgG) antibodies against Tamm-Horsfall protein were found in 51 percent of challenged (urine or Tamm-Horsfall protein) rabbits with tubulointerstitial nephritis as compared with only 8 percent of those without it (p less than 0.001). Second, in a porcine model of reflux nephropathy, 16 of 21 pigs with pyelographic findings indicative of reflux had elevated serum titers of anti-Tamm-Horsfall protein antibody as compared with 0 of 13 with normal pyelograms. Five of 10 refluxing pigs tested also had circulating lymphocytes that were cytotoxic in the presence of Tamm-Horsfall protein as compared with 0 of 13 with normal pyelograms. Third, in human studies, 12 of 49 patients with recurrent nephrolithiasis demonstrated abnormal elevations in anti-Tamm-Horsfall protein antibody; 13 of 49 had an abnormality in one of two assays of cell-mediated immunity to Tamm-Horsfall protein as compared with 0 of the normal control subjects. These abnormalities were not associated with overt obstruction or bacteriuria, but appeared to be more common in patients with recent onset and active recurrent nephrolithiasis. Lastly, an inhibitor of the binding reaction between human Tamm-Horsfall protein and its IgG antibody was detected in extracts of three uropathic coliforms. The inhibitors were partially purified by chromatographic means. Preliminary immunoautoradiographic studies revealed three or less protein-containing subunits of Escherichia coli that cross-reacted with anti-Tamm-Horsfall protein antibody. These studies suggest that autoimmune responses to Tamm-Horsfall protein may occur after exposure to Tamm-Horsfall protein by intravenous challenge, urinary reflux, or recurrent nephrolithiasis. This autoimmune response to Tamm-Horsfall protein may be the pathogenetic mechanism by which these factors, including bacteriuria, contribute to chronic pyelonephritis.

Animals↗
PubMed1996

Antibodies to Tamm-Horsfall protein in patients treated with extracorporeal shock wave lithotripsy (ESWL).

The aim of this study was to determine antibodies to Tamm-Horsfall protein in patients with nephrolithiasis treated with extracorporeal shock wave lithotripsy (ESWL). The values of antibodies to Tamm-Horsfall protein were determined by direct enzyme immunoassay. No statistically significant differences (P > 0.05) were observed for the IgG and IgM classes of antibodies between the groups of healthy subjects and patients with nephrolithiasis before, and 30 and 60 days after ESWL. The values of IgA class determined 30 days after treatment were significantly higher (P < 0.05) in patients, which could be due to the stimulation of the immune system. The highest values of antibodies to Tamm-Horsfall protein were obtained in both groups in the test with secondary antibodies directed toward IgM class, implicated at the presence of cross-reactive antibodies. Determination of antibodies to THP subunits isolated form urine of patients with nephrolithiasis should be performed.

Adult↗
PubMed2006

Diabetes mellitus and hypertension associated with shock wave lithotripsy of renal and proximal ureteral stones at 19 years of followup.

PURPOSE: SWL has revolutionized the management of nephrolithiasis and it is a preferred treatment for uncomplicated renal and proximal ureteral calculi. Since its introduction in 1982, conflicting reports of early adverse effects have been published. However, to our knowledge the long-term medical effects associated with SWL are unknown. We evaluated these adverse medical effects associated with SWL for renal and proximal ureteral stones. MATERIALS AND METHODS: Chart review identified 630 patients treated with SWL at our institution in 1985. Questionnaires were sent to 578 patients who were alive in 2004. The response rate was 58.9%. Respondents were matched by age, sex and year of presentation to a cohort of patients with nephrolithiasis who were treated nonsurgically. RESULTS: At 19 years of followup hypertension was more prevalent in the SWL group (OR 1.47, 95% CI 1.03, 2.10, p = 0.034). The development of hypertension was related to bilateral treatment (p = 0.033). In the SWL group diabetes mellitus developed in 16.8% of patients. Patients treated with SWL were more likely to have diabetes mellitus than controls (OR 3.23, 95% CI 1.73 to 6.02, p <0.001). Multivariate analysis controlling for change in body mass index showed a persistent risk of diabetes mellitus in the SWL group (OR 3.75, 95% CI 1.56 to 9.02, p = 0.003). Diabetes mellitus was related to the number of administered shocks and treatment intensity (p = 0.005 and 0.007). CONCLUSIONS: At 19 years of followup SWL for renal and proximal ureteral stones was associated with the development of hypertension and diabetes mellitus. The incidence of these conditions was significantly higher than in a cohort of conservatively treated patients with nephrolithiasis.

Adolescent↗
PubMed1983

Juvenile renal stone disease: a study of urinary promoting and inhibiting factors.

Urinary excretion of the most widely studied renal stone promoting (calcium, oxalate, uric acid and phosphate) and inhibiting (citrate, magnesium, pyrophosphate and glycosaminoglycans) factors, as well as the Tamm-Horsfall mucoprotein, was evaluated in 14 children with idiopathic calcium nephrolithiasis, 6 children with renal stone disease secondary to excretory malformations and 19 normal controls. No statistically significant differences in urinary excretion of promoting and inhibiting factors were found in children with idiopathic calcium nephrolithiasis but the relationship between promoting and inhibiting factors was changed as shown by an abnormal ratio of oxalate/citrate X glycosaminoglycans. This finding suggests that there is an imbalance between promoting and inhibiting factors in children with idiopathic calcium nephrolithiasis, and it is not detected by assay of each single substance.

Adolescent↗
PubMed1991

Etiology and treatment of urolithiasis.

Nephrolithiasis is a heterogeneous disorder, with varying chemical composition and pathophysiologic background. Although kidney stones are generally composed of calcium oxalate or calcium phosphate, they may also consist of uric acid, magnesium-ammonium phosphate, or cystine. Stones develop from a wide variety of metabolic or environmental disturbances, including varying forms of hypercalciuria, hypocitraturia, undue urinary acidity, hyperuricosuria, hyperoxaluria, infection with urease-producing organisms, and cystinuria. The cause of stone formation may be ascertained in most patients using the reliable diagnostic protocols that are available for the identification of these disturbances. Effective medical treatments, capable of correcting underlying derangements, have been formulated. They include sodium cellulose phosphate, thiazide, and orthophosphate for hypercalciuric nephrolithiasis; potassium citrate for hypocitraturic calcium nephrolithiasis; acetohydroxamic acid for infection stones; and D-penicillamine and alpha-mercaptopropionylglycine for cystinuria. Using these treatments, new stone formation can now be prevented in most patients.

Humans↗
PubMed1993

Renal stone disease in autosomal dominant polycystic kidney disease.

Nephrolithiasis is an important manifestation of autosomal dominant polycystic kidney disease (ADPKD), which occurs in approximately 20% of patients. It should always enter the differential diagnosis of flank pain in patients with ADPKD. The diagnosis is hindered by the distorted anatomy of the polycystic kidneys and the frequent occurrence of parenchymal and cyst wall calcifications, and requires demonstration of the relationship to the collecting system by intravenous urography and/or computed tomography. Computed tomography is the most sensitive imaging technique for detection of stones or calcifications, whereas intravenous urography is the most sensitive for visualization of the intrarenal collecting system. Precaliceal tubular ectasia can be detected in 15% of patients with ADPKD and nephrolithiasis, but this association may not be specific to ADPKD. The composition of the stones is most frequently uric acid and/or calcium oxalate. Metabolic factors are important in their pathogenesis. Distal acidification defects may be important in a few patients, while an abnormal transport of ammonium, low urine pH, and hypocitruria are the most common abnormalities. The treatment of nephrolithiasis in patients with ADPKD is not different from that in patients without ADPKD. Extracorporeal shock wave lithotripsy and percutaneous nephrostolithotomy in patients with early disease and normal renal function are not contraindicated.

Adult↗