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Results for “Nephrolithiasis”

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At least 127 records · Page 7Linked to original sources

PubMed1992

[Pharmacological modifications of radiation methods for studying the kidneys in determining the nature of the stenosis of the pelviureteral segment in patients with nephrolithiasis. Its outpatient diagnosis].

As many as 17 nephrolithiasis and 6 hydronephrosis patients with surgically verified irreversible (n = 13) and reversible (n = 10) stenosis of the pelviureteral segment were examined. To distinguish the character of the stenosis, use was made of excretory urography and dynamic scintigraphy with progesterone, ultrasound, and dynamic scintigraphy with furosemide. In nephrolithiasis patients, dynamic scintigraphy is less informative as compared to other modifications. As compared to hydronephrosis patients, all the modifications indicated are less informative in nephrolithiasis patients in differentiating the character of the stenosis.

Adult↗

PubMedDate not supplied

[A nephrologist's tasks in nephrolithiasis].

The epidemiological impact of nephrolithiasis stems from a significant and increasing prevalence in western countries. While the kidney is the end-organ of the disease, the causes are often more general, including metabolic derangements, pri-mary diseases of other organs and systems, hereditary renal or non-renal defects. In this context, nephrological expertise is highly recommended and could considerably improve disease outcomes. The nephrologist's involvement should start while the patient is acutely affected by renal colic. In this setting medical intervention is aimed at counteracting pain, favoring progression in the urinary tract, and preventing renal injury. The choice for urological procedures should take into account the potential for harmful effects of obstruction, infection, and prolonged pain. After the patient has undergone non-invasive procedures medical intervention improves the management of residual fragments, reduces the risk of stone recurrence, and increases compliance to the stone center, as a premise for considering patients for metabolic evaluation and subsequent medical treatment. Current study protocols, including chemistries, physicochemistry and possibly genetics, are the basis for a rational treatment of recurrent stone disease. Secondary nephrolithiasis caused by systemic disorders is screened out and treated specifically. Hereditary forms can be identified by genetic analysis and strictly followed and treated. While medical therapy can cure some types of renal stones, prolonged remission is seldom obtained in calcium nephrolithiasis. However, recurrence rates are greatly reduced, and this lessens the need for urological procedures, risk of infection/obstruction and, ultimately, progression to renal insufficiency. In the face of a multidisciplinary approach to renal stone disease, the nephrologist has a key role in the successful management of these patients.

Humans↗

PubMed2005

[Treatment of the lower pole nephrolithiasis].

BACKGROUND: The purpose of the study was to compare the efficacy of extracorporeal shock wave lithotripsy and percutaneous nephrolithotomy for lower pole nephrolithiasis. METHODS AND RESULTS: We retrospectively analyzed results of lower pole nephrolithiasis treatment in 396 patients (221 treated by extracorporeal shock wave lithotripsy and 175 by percutaneuos nephrolithotomy). We evaluated results of the treatment in the 3 months interval after the procedure in groups classified according to the stone size: <10 mm, 10-20 mm, >20 mm. Stone free status was achieved in these groups after 96 (66%), 43 (38 %) and 2 (25%) shock wave lithotripsies and 48 (84%), 75 (76%) and 25 (74%) percutaneous nepholithotomies. The efficacy irrespective of insignificant residual fragments (< 4 mm) was in 176 (66%) lithotripsies and 156 (82%) single percutaneuos nephrolithotomies. CONCLUSIONS: Percutaneous nephrolithotomy is more effective methods in the treatment for lower pole nephrolithiasis than extracorporeal shock wave lithotripsy especially for stone size >10 mm.

Adolescent↗

PubMed2005

[Multifactorial disorder: molecular and evolutionary insights of uric acid nephrolithiasis].

Nephrolithiasis is a common multifactorial disorder affecting about 10% of the Western populations and it is characterized by the presence of small crystals and stones in the urinary tract. Uric acid nephrolithiasis (UAN) accounts for 20% of all stones but its prevalence varies between countries. Nephrolithiasis is likely caused by several factors but a genetic component has clearly been demonstrated. While studying an ancient founder population in Sardinia, we recently identified a susceptibility locus for UAN on chromosome 10. In this region we identified a missense mutation in a specific isoform of a novel gene is strongly associated with UAN. Through a comparative genomic approach, we did not found a mouse homolog even if we were able to identify the corresponding genomic region, while in Old World monkey we found a canonical gene structure with several stop codons preventing protein production. We detected expression in New World monkeys while in humans we observe a functional protein. It seems, therefore, that, to avoid human disease, a fierce selection worked to develop a renal-haematic urate homeostasis system against excessive hyperuricaemia. ZNF365 emerged during primate evolution and assumed its role in parallel with the disappearance of uricase, probably against a disadvantageous excessive hyperuricaemia.

Animals↗

PubMedDate not supplied

[Total urinary protein in different types of nephrolithiasis].

In 26 healthy individuals and 114 patients with urolithiasis, total urine protein levels were measured in a single sample by using the stain ponceau S. The findings were statistically analyzed. The levels of the protein were found to be 27-80 mg/l in the healthy individuals, while the distribution of the data was asymmetric as viewed from high values. The patients with urolithiasis exhibited their protein levels according to the type of nephrolithiasis. Proteinuria was demonstrated to be less pronounced in patients with oxalate and urate nephrolithiasis than in patients with coral phosphate calculi. There was a substantial asymmetry in the distribution of total urine protein for all the examined groups of urolithiasis patients, as well as great dispersion values, which fails to regard the parameter alone as a diagnostic criterion for the type of nephrolithiasis. At the same time it was noted that simultaneous examination of the levels of total protein, uric acid, potassium, and sodium enabled the type of a concrement (oxalate or phosphate) to be in vivo estimated with approximately 85% probability.

Adult↗

PubMed1990

[The effect of oral calcium loading on the serum concentrations and urinary excretion of uric acid in patients with recurrent calcium nephrolithiasis and hypercalciuria].

The authors have established that to higher calciuria in patients with calcium nephrolithiasis correspond higher vales of uric acid serum concentrations and urine excretion than in the controls. In the oral calcium tolerance test a significant correlation was found between the changes in the uric acid urine excretion and those in the diuresis. The following conclusions are put forward. I. In the patients with recurrent calcium nephrolithiasis and hypercalcinosis one should look for active impairment of uric acid metabolism which should be kept in mind when an antirecurrence treatment is planned. 2. The established parallel increase of uricosuria and calciuria in the oral calcium tolerance test means that to patients with recurrent calcium nephrolithiasis and gout a rich calcium diet should not be prescribed since it increases the risk of formation of calcium oxalate stones.

Administration, Oral↗

PubMedDate not supplied

[The proteolysis-ion theory of the pathogenesis of nephrolithiasis].

A study was made of urinary proteolysis. This parameter turned to be decreased in patients with nephrolithiasis versus normal subjects. The authors developed an original proteoclastic-ion theory of nephrolithiasis pathogenesis, based on the two main risk factors triggering the disease: low levels of urinary proteolysis leading to the formation of a calculous matrix; the urine pH values optimal for the sedimentation of lithiasic salts. The combination of both risk factors was responsible for the development of calculous crisis and the formation of microlith. The decreased index of urinary proteolysis calculated with the formula offered could be regarded as a risk indication to the microlith formation. A possible elimination of the both risk factors was demonstrated. The technique of microlithiasis metaphylaxis was developed with regard to the major and minor risk factors and the possibility of their elimination. The values of urinary proteolysis were the criteria for a successful therapeutic response. With regard to the number of risk factors the risk of primary nephrolithiasis or lithiasis relapses could be predicted.

Crystallization↗

PubMed1987

[Calcitonin and glucagon secretion in active nephrolithiasis].

In 76 patients with active nephrolithiasis and in 28 normal subjects the influence of an Ca-load on the calcitonin and glucagon secretion and on the serum calcium, phosphate and magnesium levels was examined. In the patients with active nephrolithiasis a significant suppression of Ca-induced calcitonin secretion and absence of glucagon secretion was found. Simultaneously the patients showed a lower decrease of serum Mg and reduced increase of serum phosphate levels. The authors suggest participation of the above mentioned biochemical and endocrine abnormalities in the pathogenesis of the active nephrolithiasis.

Adult↗

PubMed1982

[Triamterene induced nephrolithiasis (author's transl)].

Various studies have demonstrated a relationship between nephrolithiasis and the ingestion of certain drugs. We are particularly interested in the effects of triamterene. Five published case studies on patients of both sexes between 43 and 60 years of age have proven that a regular consumption of normal doses of triamterene has a direct effect upon the formation of renal stones. The stones analysed by infra-red spectrophotometry during the above observations contained from 20 to 100% of triamterene and it's metabolite hydroxytriamterene, following a daily consumption of 150 to 350 mg during a period of 6 to 38 months. It has been confirmed that triamterene and it's metabolite hydroxytriamterene are very poorly soluble and super-saturate the urine for a brief period following the ingestion of the drug. Triamterene might also intervene in the initial phenomena of nucleation. It is therefore recommended that triamterene be used with caution in those patients presenting a history of nephrolithiasis. The existence of drug induced nephrolithiasis reinforces the importance of the technique of renal stone analysis, and the necessity of a systematic study of all renal stones found. This will allow us to develop the study of the correlations between the different episodes of renal stone disease, the nature of the treatment undertaken and the systematic analysis, layer by layer, of the stone.

Adult↗

PubMed1995

Dry extracorporeal shock wave lithotripsy for treatment of ureterolithiasis and nephrolithiasis in a dog.

A second-generation lithotriptor was used to perform dry extracorporeal shock wave lithotripsy in a dog with ureterolithiasis, nephrolithiasis, and chronic renal failure. Previous studies on the use of lithotripsy in dogs have involved first-generation machines and have primarily concentrated on acute and chronic effects of lithotripsy in experimental models. Treatment in this dog resulted in resolution of ureteral obstruction, ureterolithiasis, and nephrolithiasis, and avoided complications associated with ureteral and renal surgery. The only complication was substantial hematuria of 12 hours' duration immediately after the procedure. Second-generation lithotripsy may offer an effective treatment for ureterolithiasis or nephrolithiasis in selected dogs.

Animals↗

PubMedDate not supplied

[The etiological and pathogenetic bases of nephrolithiasis].

A new outlook on etiology and pathogenesis of nephrolithiasis regards renal tubular acidosis (RTA) as the basic pathogenetic factor of nephrolithiasis. These conclusions were made basing on the findings on blood and urine glycolysis enzymes, lactic acid, acid-base metabolism, titrated acids, ammonium. RTA stages responsible for the variety of the forming concrement and two groups of nephrolithiasis etiological factors (acting on epithelial cell of the nephron and involved in urinary processes) are distinguished.

Acid-Base Equilibrium↗

PubMedDate not supplied

[Lipid peroxidation in the kidney tissue of patients with nephrolithiasis and chronic pyelonephritis].

Lipid peroxidation (LPO) activity has been analyzed in homogenates and microsomes of cortical samples obtained intraoperatively from the kidneys of 33 patients. Of them, 21 patients had mild, moderate or severe pyelonephritis or nephrolithiasis. Unaffected cortical tissue from renal carcinoma patients was used as control. LPO activity was judged by basal level of malonic dialdehyde (MDA) and MDA growth in the homogenate and microsomes following initiation of ascorbate-dependent LPO. Activation of LPO was registered in patients with moderate disease with active inflammation. They also exhibited greater MDA basal levels and rapid MDA increase in response to in vitro initiation of ascorbate-dependent LPO simultaneously with attenuation of endogenous antioxidant defense. In severe pyelonephritis and nephrolithiasis with drastic deficiency of renal function LPO activity was low and nonresponsive to stimulation either by ascorbate or Fe+2. This is probably due to lack of the substrate after massive death of renal cells. Enhancement of LPO activity in patients with pyelonephritis or nephrolithiasis against functioning kidneys may appear responsible for destruction of renal tissue.

Adolescent↗

PubMed1997

Clinical and biochemical patterns of presentation in monolateral and bilateral calcium nephrolithiasis.

To investigate patterns of monolateral and bilateral nephrolithiasis, we enrolled 196 patients with idiopathic calcium stone disease (ICaSD) and 36 with proven primary hyperparathyroidism (PHP). Monolateral disease occurred in 45 subjects with ICaSD and 3 with PHP. All had had three or more stone events. They were studied for a number of clinical and biochemical parameters. The expected prevalence of monolateral stone disease was calculated according to the binomial distribution of random events. Whereas the observed and expected prevalence of monolateral nephrolithiasis did not differ in PHP, the distribution did not follow a chance pattern in ICaSD, since monolateral disease was still frequent among patient with more than 6 episodes. To find out whether monolateral and bilateral ICaSD had distinct pathogenic mechanisms the two groups were compared for clinical and biochemical patterns: no differences emerged concerning metabolic derangements, urine saturation and diet-related biochemistries. Bilateral stone-formers had a higher recurrence rate, but a similar number of stone-operations or ESWL. In 81 of 151 bilateral idiopathic stone-formers in which we were able to assess the exact number of stone events in left and right kidney, the distribution of stones between kidneys did not differ from the binomial distribution. In conclusion, while PHP-associated nephrolithiasis presents predictable patterns, ICaSD comprises a subset in which the disease occurs monolaterally. These forms cannot be distinguished from bilateral forms with common clinical features or routine biochemistries.

Age of Onset↗

PubMedDate not supplied

[Lipid peroxidation and Ca-dependent ATPase activity in the microsomal fraction of renal tissue in patients with nephrolithiasis and chronic pyelonephritis].

The author has estimated levels of malonic dialdehyde (MDA) indicative of activity of membrane phospholipid peroxidation activity, basal and true (in incubation in the culture containing glomeruloform antibiotic alameticin) Ca-ATPase activity in microsomal fraction isolated from cortical tissue of functioning kidneys obtained intraoperatively from 26 patients. 12 samples of cortical tissue obtained from uninvolved parts of the kidneys affected with carcinoma served as control. 14 samples were obtained from the tissue of functioning kidneys affected with nephrolithiasis and active chronic pyelonephritis. The investigations show elevated MDA levels, enhanced basal in reduced true Ca-ATPase activity of microsomes from the kidneys of patients with nephrolithiasis and active chronic pyelonephritis compared to control. It is suggested that high basal against low true Ca-ATPase activity of renal microsomes may be explained by increased permeability of renal membranes for Ca2+ under activation of lipid peroxidation in active chronic pyelonephritis and nephrolithiasis.

Adolescent↗

PubMedDate not supplied

Cystic fibrosis and calcium oxalate nephrolithiasis.

During the past six years, we have treated eight patients with cystic fibrosis (CF) for nephrolithiasis. In seven patients, the stones were comprised of calcium oxalate. Another six patients had calcium oxalate crystalluria. In our CF population of 140 patients, this represents a cumulative incidence of calcium oxalate nephrolithiasis of 5.7 percent and an additional 4.2 percent incidence of crystalluria. Experience with these patients is reviewed. Pancreatic insufficiency was universally associated with nephrolithiasis or crystalluria. Diabetes and cirrhosis were also common. Predisposing factors and potential mechanisms of stone disease in pancreatic insufficient CF patients are discussed, focusing on the relationship between fat malabsorption in CF to oxalate metabolism.

Absorption↗

PubMed1997

Calciotropic hormones and nephrolithiasis.

In recurrent calcium stone formers interfering factors or changes in receptor sensitivity may alter the interrelationships among calcium-regulating hormones, and hormonal behavior often does not fit with the theoretical assumptions. The vitamin D system appears to have the most important metabolic and clinical effects. Abnormal up-regulation of the synthesis of calcitriol and the consequent parathyroid hormone (PTH) suppression can induce hypercalciuria. Consequently, the hypocalciuric effect of thiazide would be caused by an enhanced response to PTH and by a reduction in 1,25(OH)2-vit D. A negative role of vitamin D on the skeleton has been observed in the presence of a negative calcium balance. Moreover, vitamin D also plays a role in urine oxalate excretion. PTH seems not to be directly stimulated in hypercalciuria and recurrent calcium nephrolithiasis, and patients with hyperparathyroidism and recurrent calcium nephrolithiasis show a similar degree of bone demineralization, irrespective of the presence of absence of the so-called 'primary hyperparathyroidism.' Calcitonin plays a contributory role in the pathogenesis of recurrent calcium nephrolithiasis that seems to be strictly related to dietary calcium intake. A higher sensitivity of thyroid C cells, particularly in absorptive hypercalciuric patients, could be related to the pathogenesis of hypercalciuria and contribute to its persistence.

Calcitonin↗

PubMed2006

An unusual patient with hypercalciuria, recurrent nephrolithiasis, hypomagnesemia and G227R mutation of Paracellin-1. An unusual patient with hypercalciuria and hypomagnesemia unresponsive to thiazide diuretics.

A 19-year-old female patient with hypercalciuria and recurrent nephrolithiasis/urinary tract infection unresponsive to thiazide type diuretics is presented. The patient first experienced nephrolithiasis at the age of 4 years. Afterwards, recurrent passages of stones and urinary tract infection occurred. On diagnostic evaluation at the age of 19 years, she also had hypocitraturia and hypomagnesemia. Her serum calcium concentrations were near the lower limit of normal (8.5-8.8 mg/dl; normal range: 8.5-10.5), her serum magnesium concentrations were 1.15-1.24 mg/dl (normal range: 1.4-2.5) and urinary calcium excretion was 900 mg/24 h. PTH concentrations were increased (110-156 pg/ml; normal range: 10-65). We tried to treat the patient with hydrochlorothiazide at a dose of 50 mg/day. During treatment with thiazide diuretics, PTH concentration remained high and the patient had recurrent urinary tract infections and passages of stones. Serum magnesium concentration did not normalize even under the parenteral magnesium infusion. Her mother had a history of nephrolithiasis 20 years ago. Severe hypomagnesemia in association with hypercalciuria/urinary stones is reported as a rare autosomal recessive disorder caused by impaired reabsorption of magnesium and calcium in the thick assending limp of Henle's loop. Recent studies showed that mutations in the CLDN16 gene encoding paracellin-1 cause the disorder. In exon 4, a homozygous nucleotide exchange (G679C) was identified for the patient. This results in a point mutation at position Glycine227, which is replaced by an Arginine residue (G227R). The mother was heterozygous for this mutation. G227 is located in the fourth transmembrane domain and is highly conserved in the claudin gene family. This case indicates the pathogenetic role of paracellin-1 mutation in familial hypomagnesemia with hypercalciuria and nephrocalcinosis and further underlines the risk of stone formation in heterozygous mutation carriers.

Adult↗

PubMedDate not supplied

Acclerated calcium nephrolithiasis.

Of 674 patients with calcium nephrolithiasis, 78 formed their stones in large numbers (average, 22 stones per patient) and at an accelerated rate (average, 172 stones per 100 patient-years). Although their stone disease was unusually severe, these patients had the common metabolic causes of stones and responded well to treatment. Patients with even the most extremely active calcium nephrolithiasis should be evaluated and managed in the same way as those with the common, less active form of the disease.

Calcium↗