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PubMed1993

Nephrolithiasis in children.

A study of 100 cases of nephrolithiasis between 3 to 15 years of age is reported. Seventy four cases were more than 10 years old. The common presenting symptoms included abdominal pain (69%), burning micturition (23%), gross hematuria (4%) and unexplained pyrexia (6%). Associated urinary tract malformations were found in 16 cases. Twenty four had struvite calculi. Urinary infection with Proteus mirabilis was found in 23 children and idiopathic hypercalciuria in 31 cases. Following surgical removal, either percutaneously or by open surgery, 8 patients had residual calculi and in 6 cases recurrence occurred.

Adolescent↗

PubMed1976

[Nephrolithiasis in hypercalciuria and hyperparathyroidism].

In the group of 1635 patients with nephorolithiasis the authors found 16% with idiopathic hypercalciuria. They administered thiazide diuretics for 8 days as a test for the detection of masked hyperparathyroidism in idiopathic hypercalciuria. In 6 cases which were diagnosed in this manner, the existence of a parathyroidadenoma could be demonstrated by surgical operation. The hypercalciuria persisted after exstirpation of the tumor, in some cases the nephrolithiasis also remained active. the various pathogenetic mechanisms connected with these common diseases are discussed in relation to these results.

Adenoma↗

PubMedDate not supplied

[Staghorn nephrolithiasis].

The authors review the problem of staghorn nephrolithiasis (SN) basing on their experience in the disease diagnosis, treatment and prevention. Basing on the analysis of 2021 cases (1354 females and 667 males), the data on SN etiology and pathogenesis are provided. A complex of diagnostic procedures, an original classification, differentiated indications to various conservative or surgical treatments, trends in prevention of nephrolith reappearance, promising research approaches are outlined.

Adult↗

PubMed1995

Etiology of calcium oxalate nephrolithiasis in rats. I. Can this be a model for human stone formation?

Crystal retention is studied in a rat-model system as a possible mechanism for the etiology of human nephrolithiasis. A crystal-inducing diet (CID) of ethylene glycol plus NH4Cl in their drinking-water is offered to healthy rats to generate intratubular crystals. Subsequently, the fate of retained crystals is investigated by allowing the rats a tissue recovery/crystalluria phase for three, five and ten days, respectively, on normal drinking water. The process of exotubulosis is observed in cortex and medulla of aldehyde-fixed kidneys after three days recovery. After five days, crystals are predominantly seen there in the interstitium. After ten days, cortex and medulla are virtually free of crystals. However, in the papillary regions after five and ten days recovery, three types of calcium oxalate monohydrate (COM) crystals are present: (1) free in the calycine space, (2) sub-epithelially located surrounded by interstitial cells within, and (3) covered by macrophage-like cells, outside the original papillary surface. After a CID plus three days recovery, a further thirty-seven days extra oxalate challenge with solely 0.3 vol% ethylene glycol induced intratubular and interstitial oxalate crystals. In the papillary region, large sub-epithelial crystals are seen. However, no crystals are seen in kidneys from rats given solely (0.5 or 0.8 vol.%) ethylene glycol for thirty days. An oxalate re-challenge retards crystal removal.

Ammonium Chloride↗

PubMed1995

Experimental calcium oxalate nephrolithiasis and the formation of human urinary stones.

Calcium oxalate nephrolithiasis in rats requires induction of hyperoxaluria which results in increased urinary calcium oxalate supersaturation. As a result of low to mild chronic hyperoxaluria, calcium oxalate crystals deposit first in the papillary collecting ducts. Crystal deposition in the kidneys is preceded by calcium oxalate crystalluria and starts with the retention of aggregated calcium oxalate crystals in the renal tubules. Retained crystals move from the tubules to the interstitium, and in the process, become anchored to the tubular basement membrane. Crystal aggregates present in the superficial peripheral collecting ducts of the renal papillae ulcerate through to the papillary surface and grow into the stones.

Animals↗

PubMed1996

Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study.

PURPOSE: We define the role of urine volume as a stone risk factor in idiopathic calcium stone disease and test the actual preventive effectiveness of a high water intake. MATERIALS AND METHODS: We studied 101 controls and 199 patients from the first idiopathic calcium stone episode. After a baseline study period the stone formers were divided by randomization into 2 groups (1 and 2) and they were followed prospectively for 5 years. Followup in group 1 only involved a high intake of water without any dietetic change, while followup in group 2 did not involve any treatment. Each year clinical, laboratory and radiological evaluation was obtained to determine urinary stone risk profile (including relative supersaturations of calcium oxalate, brushite and uric acid by Equil 2), recurrence rate and mean time to relapse. RESULTS: The original urine volume was lower in male and female stone formers compared to controls (men with calcium oxalate stones 1,057 +/- 238 ml./24 hours versus normal men 1,401 +/- 562 ml./24 hours, p < 0.0001 and women calcium oxalate stones 990 +/- 230 ml./24 hours versus normal women 1,239 +/- 440 ml./24 hours, p < 0.001). During followup recurrences were noted within 5 years in 12 of 99 group 1 patients and in 27 of 100 group 2 patients (p = 0.008). The average interval for recurrences was 38.7 +/- 13.2 months in group 1 and 25.1 +/- 16.4 months in group 2 (p = 0.016). The relative supersaturations for calcium oxalate, brushite and uric acid were much greater in baseline urine of the stone patients in both groups compared to controls. During followup, baseline values decreased sharply only in group 1. Finally the baseline urine in patients with recurrences was characterized by a higher calcium excretion compared to urine of the patients without recurrences in both groups. CONCLUSIONS: We conclude that urine volume is a real stone risk factor in nephrolithiasis and that a large intake of water is the initial therapy for prevention of stone recurrences. In cases of hypercalciuria it is suitable to prescribe adjuvant specific diets or drug therapy.

Adult↗

PubMedDate not supplied

[A familial form of nephrolithiasis in patients following kidney transplantation?].

Causes and mechanisms underlying nephrolithiasis after transplantation of the kidney differ much from known in other urological patients. We have found calculi in transplanted kidney in 5 of 939 surgical patients. Two cases of concrement formation in the transplant in the members of the same family aged 22 and 26 years we report as interesting. Our experience and literature data suggested family nature of the concrements. One of the patients underwent pyelolithotomy, the other impulse lithotripsy. Both the transplants function normally 5 years after kidney transplantation.

Adult↗

PubMed1996

Interaction of urinary crystals with renal epithelial cells in the pathogenesis of nephrolithiasis.

Renal tubular fluid in the distal nephron is supersaturated with calcium and oxalate ions that nucleate to form crystals of calcium oxalate monohydrate (COM), the most common crystal in renal stones. It is not known how these nascent crystals are retained in the nephron to form calculi in certain individuals. Recent studies from this laboratory indicate that COM crystals can bind within seconds to anionic, sialic acid-containing glycoproteins on the apical surface of kidney epithelial cells in culture, suggesting one mechanisms whereby crystals could be retained in the tubule. Adherence of crystals to renal epithelial cells is inhibited by specific urinary anions such as glycosaminoglycans, uropontin, nephrocalcin, and citrate, each of which binds to the crystalline surface. Thus competition for the crystal surface between soluble anions in tubular fluid and anions on the apical cell surface could determine whether or not a crystal binds to the cell. Once bound, crystals are quickly internalized by renal cells in culture; reorganization of the cytoskeleton, alterations in gene expression, and initiation of proliferation can then ensue. Each of these cellular events appears to be regulated by a different set of extracellular factors. Identification of molecules in tubular fluid and on the cell surface that modulate crystal-cell interactions, as well as their mechanism of action, appears critical for understanding the pathogenesis of nephrolithiasis.

Calcium Oxalate↗

PubMed1996

Nephrolithiasis as a presenting feature of chronic sarcoidosis: a prospective study.

BACKGROUND AND AIM OF THE WORK: The presentation of sarcoidosis with renal stones has never been evaluated in a prospective study. DESIGN: We have studied 110 consecutive patients with histologically proven sarcoidosis, first seen in the years 1993-1994 in the Milan Sarcoid Clinic. Those who had renal stones preceding or suggesting the diagnosis of sarcoidosis, and those who had evidence of renal calculi at presentation, were studied up to 31 December 1995 with serial evaluation of calcaemia, calciuria and serum 1,25 (OH)2D3 and are the basis of this report. RESULTS: Four patients had had calculi a long time ago and probably unrelated to their sarcoidosis. Three patients had a previous history of recurrent colic with calculi. In one further patient the occurrence of calculi suggested the diagnosis. In three other patients pyuria or microscopic haematuria at the presentation of pulmonary sarcoidosis led to the diagnosis of asymptomatic calculi. All the above seven patients had features of chronic disease and required long term corticosteroid therapy. Four of them required lithotripsy or pyelotomy before starting steroid therapy. Another had further calculi during the follow-up, and an episode of hydronephrosis requiring lithotripsy, due to poor compliance to corticosteroid therapy. Another patient had a single stone during follow-up in spite of proper therapy. In all the others prednisone was useful to control the disease. Summing up the results of a previous similar but retrospective study from our clinic, we can describe the full spectrum of nephrolithiasis at presentation of sarcoidosis, as it appears from the examination of 729 consecutive patients seen over 17 years (1978-1994), with a further follow-up of at least one year (see Conclusions). CONCLUSIONS: 1. Renal stones may be the presentation of sarcoidosis in 3.6% of cases, but the etiology may go unrecognized for many years in most of them. 2. There are asymptomatic renal stones at presentation in a further 2.7%: pyuria or microscopic haematuria may suggest such an occurrence. 3. Renal calculi appear to be a marker of chronicity, with long term corticosteroid therapy required in most cases. 4. A diagnosis of sarcoidosis should always be considered when patients present with renal calculi of unknown origin.

Adult↗

PubMed1997

Lipid peroxidation in ethylene glycol induced hyperoxaluria and calcium oxalate nephrolithiasis.

PURPOSE: To determine if lipid peroxidation plays a role in renal injury associated with experimental nephrolithiasis. MATERIALS AND METHODS: Hyperoxaluria was produced in rats by ethylene glycol in drinking water. At 15, 30 and 60 days of treatment, urinary oxalate, lipid peroxide, calcium oxalate crystals, enzymes and tissue lipid peroxide were measured. RESULTS: Urinary oxalate increased significantly at all time periods and was associated with crystalluria. Lipid peroxides in kidney tissue and urine increased at all time periods. Tissue calcium oxalate crystal deposits from 0 to 1+ were present on day 15, but present in all animals on days 30 and 60. Renal tubular cell damage was confirmed by an increase in urinary marker enzymes. CONCLUSIONS: Renal cell damage is associated with lipid peroxide production indicating cell injury due to the production of free radicals. The damage appears due primarily to hyperoxaluria and is augmented by crystal deposition in the renal tubules.

Animals↗

PubMed1996

[Effective treatment of nephrolithiasis of the lower calix using ESWL (evaluation of 452 procedures)].

The authors present their results with the treatment of nephrolithiasis of the lower calix using the method of extracorporeal lithotripsy with the Czech apparatus Medilit M-5. In 310 patients they made 452 operations and checked the therapeutic results three months after the last session. For checking they used a native nephrogram and examination by ultrasound. With the increasing size of concrements the effectiveness declined and thus also the success of ESWL(in concrements above 20 mm in size it declined to 30%). This is not due only to the size of the concrement but also its site in the lower calix which is unfavourable for the elimination of fragments after ESWL. The authors recommend therefore in large concrements of the lower calix (more than 20 mm in the longitudinal axis) to select as the primary method percutaneous nephrolithotomy which is highly effective in this localization and is independent on the size of the concrement. The general success rate achieved in treatment of lithiasis of the lower renal calix with Medilit M-5 is 61.3% and is comparable with other lithotriptors.

Female↗

PubMed1997

[Nephrolithiasis--rational etiological assessment].

Although underlying metabolic abnormalities do not differ fundamentally in patients with either first or recurrent nephrolithiasis and 35% of patients with a first event may have to face a recurrence 5 years later, extended metabolic investigations in patients with a first renal calculus should be restricted to particular, exceptional cases. However, in patients with a first calculus basic investigations with respect to specific causes for a concrement such as primary hyperparathyroidism, incomplete renal-tubular acidosis, recurrent urinary tract infection and cystinuria are mandatory. This includes, in addition to a laboratory investigation of blood and urine after a 2-hour-fasting period, analysis of the stone and a urography. The extended metabolic investigation in patients with recurrences or a first occurrence in a patients with a risk constellation includes evaluation of the most important lithogenic (calcium, oxalate, phosphate, uric acid) and inhibiting components (citrate) in the 24-hour urine, in patients with cystine calculi quantitation of cystine. A metabolic investigation should never be undertaken in the hospital or under standardized diet, but always under accustomed, unrestricted nutrition. At least 2 urine samples should be investigated from each patient, preferably not prior to 3-4 months after the event when homeostasis of the patient is restored analogously to the onset of concrement development.

Acidosis, Renal Tubular↗

PubMedDate not supplied

[Kidney functional status in patients with staghorn nephrolithiasis complicated by chronic kidney failure after an organ-preserving surgical intervention].

On the basis of examination of 125 patients with coral nephrolithiasis complicated by chronic renal insufficiency, who underwent various organ-sparing surgical interventions, the author has come to a conclusion that functional capacity of both the operated and the contralateral kidney gets impaired after the operation, its degree being directly related to the particular stage of chronic renal insufficiency. Adoption of an adequate antibacterial and disintoxication therapy in combination with hemodialysis (if indicated) in the postoperative period permit improving not only the functional state of the two kidneys but also the outcome of the organ-sparing surgical intervention.

Anti-Infective Agents↗

PubMed1996

[Distal renal tubular acidosis and nephrolithiasis in 3 cases of primary Sjögren syndrome].

Tubulo interstitial nephritis, the main manifestation of renal involvement in Sjögren syndrome, may lead to a tubular dysfunction that is usually subclinical. We report three women, aged 32, 35 and 35 years old, with a primary Sjögren syndrome and symptomatic type I or distal tubular acidosis. Two patients had nephrolithiasis and one a nephrocalcinosis. Two had a basal hyperchloremic metabolic acidosis. The ammonium chloride acidification test was abnormal in all, demonstrating a distal tubular defect. None had proximal tubular dysfunction. All had an urinary pH over 6.5 and hypocitraturia and none had hypercalciuria. Renal calculi were composed of calcium oxalate and calcium phosphate in two patients and calcium phosphate and ammonium phosphate in the other. All women had positive antinuclear antibodies with mottled pattern, two had anti Ro antibodies and positive rheumatoid factor and one had hypergammaglobulinemia. None had anti La antibodies, crioglobulinemia or monoclonal proteins.

Acidosis, Renal Tubular↗

PubMed1997

Piezoelectric extracorporeal shock-wave lithotripsy of lower pole nephrolithiasis.

OBJECTIVE: To evaluate the efficacy of the EDAP LT 02 lithotriptor for the treatment of lower pole nephrolithiasis. METHODS: From January 1994 to September 1995, 91 patients presenting with solitary radiopaque calculi of the lower pole calix were treated by piezoelectric extracorporeal shock-wave lithotripsy (ESWL) with the EDAP LT 02. Among them, 82 were available for follow-up. The stones' largest diameter of these patients varied from 5 to 15 mm (mean = 8.1). Indications for ESWL were pain in 63 (77%), hematuria in 5 (6%), associated infection in 6 (7.5%) and stone size in 8 (10%) asymptomatic patients. Stone localization was assessed as very easy in 74 cases (90%) and difficult in 8 cases (10%) but no intraoperative IVP was needed. ESWL sessions were performed with intravenous sedo-analgesia in 69 cases (80%) and general anesthesia in 17 cases (20%). After ESWL we advised patients to combine a diuresis with postural drainage. RESULTS: Most patients were treated with one session of ESWL: none required more that two (mean = 1.05). The mean hospital stay for one session was 1.2 +/- 0.7 days. Obstructive complication rate was 11% and auxiliary treatments were necessary in 6%. The stone-free rate of in situ piezoelectric ESWL monotherapy was overall 84%, and 95% of patients with pain were cured. CONCLUSION: In the absence of abnormality of the upper urinary tract, the vast majority of small lower pole caliceal stones can be completely removed by piezoelectric ESWL without recourse to more invasive methods.

Adult↗

PubMedDate not supplied

[The effect of extracorporeal shockwave lithotripsy on the indices of urinary enzymes in nephrolithiasis patients].

Immediate and long-term effects of extracorporeal shock-wave lithotripsy (ESWL) on urine enzymes were studied in 200 patients with nephrolithiasis (NL). The patients had abnormally high urine excretion of AP, GGT, APA, LDH and NAG, whereas aminotransferases excretion was low. Pathobiochemical and diagnostic implications of these findings are discussed. Immediately after its conduction ESWL entails a mild injury to tubular portion of the nephron. The causes of long-term stay of enzymuria after ESWL in NL patients are discussed.

Adult↗

PubMedDate not supplied

[Effects of shock-wave lithotripsy (ESWL) on electrolytic and hormonal balance in nephrolithiasis patients].

Blood concentrations of parathyroid hormone, aldosterone, hydrocortisone, Na+, K+, Ca2+, 24-h urine concentration of Ca2+, blood pressure were measured on day 3 and 7 after extracorporeal shock-wave lithotripsy. A total of 54 patients with nephrolithiasis (NL) were examined. In NL patients with hypertension the above lithotripsy led to a fall in pressure by 15-20%, to correction of initial hormonal and electrolytic unbalance. There were marked changes in the levels of parathyroid hormone, total Ca2+ in the blood and 24-h urine.

Adult↗

PubMed1976

Renal tubular defects in recurring bilateral nephrolithiasis.

A metabolic study was performed in 28 patients with bilateral recurrent calcium-containing renal staghorn calculi and chronic pyelonephritis ("obstructive nephropathy"). Fourteen had normal GFR and 14 mild renal insufficiency. Ten normal subjects were used as controls. Under basal conditions, polyuria and negative sodium balance were commonly observed in patients with obstructive nephropathy and normal renal function. After an acute acid load (NH4Cl) an acidifying defect, i.e. high values for urine pH and reduced excretion of titratable acid and ammonium, was observed in 64% of patients with normal GFR and in 71.4% of those with renal insufficiency. During intravenous infusion with neutral sodium phosphate, the urine pH changed little but the rate of excretion of titratable acid increased in direct proportion to that of urinary phosphate in both groups of patients. These results, associated with the finding of normal blood pH in almost all patients, lead to the conclusion that an incomplete Type 1 or "distal" renal tubular acidosis is a frequent complication of obstructive nephropathy secondary to bilateral nephrolithiasis. The anatomical abnormalities of renal tubules and collecting ducts and the superimposed interstitial nephritis might be the pathogenetic factors responsible for the acidifying defect and for the impairment in sodium and water conservation.

Acidosis, Renal Tubular↗