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Query: UMLS:C0451641 (
urolithiasis
)
3,973
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In renal exploratory excisions the isoenzyme C of the
carbonic anhydrase
was detected in 51 operative treated patients with recurrent
urolithiasis
and in 6 patients with ren mobilis or stenosis of the ureteral pelvic junction by using the immunohistochemical PAP-method. In the distal tubules and collecting ducts there is an alternating occurrence of cells with small and those with strong reactivity. This correlates with the distribution of mean or principal (P-, small reaction) and intercalated (I-, strong reaction) cells. The number of
carbonic anhydrase
rich cells and the degree of their cytoplasmic reaction to this enzyme seem to correlate with the ability of the urine to acidify. The patients were divided into four groups according to the mean urine pH estimated for a period of two weeks. The third group with predominantly acid urine (pH less than 5.8) showed a significantly increased number of
carbonic anhydrase
rich cells (mean = 63% +/- 6, n = 18) as compared to the first group (controls) without
urolithiasis
and normal urine (pH 5.8-6.8, mean = 46% +/- 8, n = 6) or the second group with
urolithiasis
and normal urine (pH 5.8-6.8, mean = 46% +/- 8, n = 28). The fourth group with predominant alkaline urine (pH greater than 6.8) showed a significantly decreased number of intercalated cells (mean = 42% +/- 16, n = 5) in comparison to the third group. Indeed, the difference with the control group is not significant but the cytoplasmic reaction of I-cells decreases distinctly in comparison to all other groups.
...
PMID:Immunohistochemical detection of renal carbonic anhydrase of patients with recurrent urolithiasis. 190 89
The enzyme
carbonic anhydrase
was detected with an indirect immunoperoxidase method in 22 kidney exploratory excisions of patients with
urolithiasis
, ren mobilis or stenosis of ureteral pelvic junction. The reactivity of
carbonic anhydrase
was related to disturbances in acid-base equilibrium. Carbonic anhydrase was detected in the convoluted parts of the distal tubules, connecting tubules and cortical collecting ducts. The distribution corresponds vastly with the localization of intercalated cells. The reaction was increased in three cases with acid rigidity and was strongly reduced in one case of renal tubular acidosis.
...
PMID:[Detection of carbonic anhydrase in the human kidney from the viewpoint of acid-base regulation (an immunohistochemical study in urolithiasis patients)]. 641 Jun 13
Drug-induced
urolithiasis
are observed in 1.6% of the urinary calculi in France. Drugs crystals are identified in two thirds of these stones. Other drugs are responsible for stones which have an apparent metabolic origin (one third of the cases). Stone analysis using physical methods such as infrared spectroscopy is needed to unambiguously identify stones containing drugs. The inquiry is an important step to identify lithogenetic drugs which do not crystallize in the stones. The main substances which were identified in stones over the past decade were indinavir monohydrate (31.4%), triamterene (11.1%), sulphonamides (10.5%) and amorphous silica (4.5%). The main drugs involved in the nucleation and growth of metabolic stones were calcium and vitamin D supplementation (15%) and long-term treatment with
carbonic anhydrase
inhibitors (8%). Stone prevention is based on drug withdrawal or change in dosage with additional measures including an increase of diuresis and, if necessary, changes in the urine pH.
...
PMID:[Drug-induced urinary calculi in 1999]. 1065 46
Exfoliated human urinary tract epithelial cells and renal tubular cells from urinary sediments of healthy adults, of urological patients and of internal patients were isolated and cultured. Cells started proliferating within 1 week after seeding a sediment. Proliferating cells formed colonies of different morphologies, designated as type-1 or type-2 cell colonies. Type-1 cell colonies showed irregular contours and spindle-like cells within the colonies. Subcultivation of type-1 cells for up to six passages was possible. Type-2 cell colonies showed smooth-edged contours and subcultivation was not possible. The epithelial character of type-1 cells was demonstrated by positive immunohistochemical staining for cytokeratin-7. In contrast to
carbonic anhydrase
-positive stained Madin Darby canine kidney cells (MDCK), which were used as positive controls for renal tubular cells, type-1 cells were
carbonic anhydrase
-negative on staining with the cobalt phosphate method. This indicates that type-1 cells were not of renal tubular origin. Type-2 cells were positively stained for
carbonic anhydrase
, indicating that type-2 cells were renal tubular cells. Type-2 cell colonies could be assigned to two subgroups with different cell forms. Colonies of cobblestone-like cells more often occurred than type-2 cell colonies with spindle-like cells, which are described in this study for the first time. Colonies with cobblestone-like cells formed domes (hemicysts), whereas spindle-like type-2 cell colonies did not. Cultures of urinary sediments from healthy adults, elderly multimorbid patients treated with furosemide, and urological patients with
urolithiasis
treated with sulfamethoxazole/trimethoprim and/or with a percutaneous nephrostomy catheter were compared. In 52% of all cultured sediments from healthy adults, in 30% of those from multimorbid patients, and in 75-80% of those from urological patients cells proliferated to colonies. The ratios of type-1 to type-2 cell colonies were 3.3:1 (healthy adults), 1.4:1 (urological patients with
urolithiasis
), and 1.8:1 (urological patients with
urolithiasis
, urine was directly collected from the renal pelvis with a percutaneous nephrostomy catheter). Successful cultures of the urinary sediments from these three groups revealed means of 3 or 4 colonies, 14 colonies, and 21 colonies, respectively. Differences in the number of colonies in relation to sex were observed only for the group of urological patients. It was shown that type-1 cells were urothelial cells, which did not show morphological differences due to their locations of origin within the urinary tract, whereas type-2 cells were probably renal tubular cells. These findings offer new aspects in the culturing of human urothelial or kidney epithelial cells with a method based on noninvasive collecting of specimens and requiring only minimal culture effort. The cultures obtained by this method can be used for in vitro studies in toxicological and clinical research.
...
PMID:Cultures of exfoliated epithelial cells from different locations of the human urinary tract and the renal tubular system. 1120 69
Analysis of 22,510 urinary calculi between January 1991 to July 2000 performed by infrared spectroscopy allows for separation of drug-induced
urolithiasis
into two categories: first, the drugs physically embedded in the stone (n = 238; 1.0 per cent), notably indinavir monohydrate (n = 126; 52.9 per cent), followed by triamterene (n = 43; 18.1 per cent), sulphonamides (n = 29; 12.2 per cent) and amorphous silica (n = 24; 10.1 per cent); second, the category of metabolic nephrolithiasis induced by drugs (n = 140; 0.6 per cent), involving mainly calcium and vitamin D supplementation (n = 56; 40.0 per cent) and
carbonic anhydrase
inhibitors (n = 33; 23.6 per cent). Composition of the stone depended not only on the inducer drug but also on the metabolic state of the patient. Today, drug-induced stones comprise about 1.6 per cent of all calculi in France. Physical analysis and therapeutic history recall of such patients are the keys to diagnosis. Medical care is based on drug avoidance or dose adjustment with increased diuresis and, if necessary, change in urinary pH.
...
PMID:[Urinary lithiasis of medical origin]. 1187 1
Children with refractory epilepsy who are co-treated with the ketogenic diet (KD) and
carbonic anhydrase
inhibitor (CA-I) anti-epileptic medications including topiramate (TPM) and zonisamide (ZNS) are at risk for
urolithiasis
. Retrospective chart review of all children treated with ketogenic therapy at our institution was performed in order to estimate the minimal risk of developing signs or symptoms of stone disease. Children (N=93) were classified into groups according to KD+/-CA-I co-therapy. Fourteen patients had occult hematuria or worse, including 6 with radiologically confirmed stones. Three of 6 calculi developed in the KD+ZNS group of 17 patients who were co-treated for a cumulative total of 97 months (3.1 stones per 100 patient months). One confirmed stone was in the KD+TPM group of 22 children who were co-treated for a cumulative total of 263 months (0.4 stones per 100 patient months). All six patients had at least three of five biochemical risk factors including metabolic acidosis, concentrated urine, acid urine, hypercalciuria and hypocitraturia. Standard of care interventions to minimize hypercalciuria, crystalluria and stone formation used routinely by pediatric nephrologists should also be prescribed by neurologists treating patients with combination anti-epileptic therapy. Non-fasting KD initiation, fluid liberalization, potassium citrate prophylaxis as well as regular laboratory surveillance are indicated in this high risk population.
...
PMID:Urolithiasis on the ketogenic diet with concurrent topiramate or zonisamide therapy. 2046 20
In rats, we recently showed how a chronic metabolic acidosis simultaneously reduced urinary oxalate excretion and promoted oxalate secretion by the distal colon leading to the proposition that acid-base disturbances may trigger changes to renal and intestinal oxalate handling. The present study sought to reproduce and extend these observations using the mouse model, where the availability of targeted gene knockouts (KOs) would offer future opportunities to reveal some of the underlying transporters and mechanisms involved. Mice were provided with a sustained load of acid (NH
4
Cl), base (NaHCO
3
) or the
carbonic anhydrase
inhibitor acetazolamide (ATZ) for 7 days after which time the impacts on urinary oxalate excretion and its transport by the intestine were evaluated. Mice consuming NH
4
Cl developed a metabolic acidosis but urinary oxalate was only reduced 46% and not statistically different from the control group, while provision of NaHCO
3
provoked a significant 2.6-fold increase in oxalate excretion. For mice receiving ATZ, the rate of urinary oxalate excretion did not change significantly. Critically, none of these treatments altered the fluxes of oxalate (or chloride) across the distal ileum, cecum or distal colon. Hence, we were unable to produce the same effects of a metabolic acidosis in mice that we had previously found in rats, failing to find any evidence of the 'gut-kidney axis' influencing oxalate handling in response to various acid-base challenges. Despite the potential advantages offered by KO mice, this model species is not suitable for exploring how acid-base status regulates oxalate handling between the kidney and intestine.
Urolithiasis
2019 Jun
PMID:Oxalate transport by the mouse intestine in vitro is not affected by chronic challenges to systemic acid-base homeostasis. 2994 93
