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Biomedical subjects

G P Kasidas

Publications and source records attributed to G P Kasidas.

At least 19 recordsLinked to original sources
PubMed2004

Renal stone analysis: why and how?

Upper urinary tract stone disease is widespread in the developed world. On both clinical and economic grounds it is now accepted that evidence-based medical intervention is the only approach likely to make a significant impact on the incidence, and more importantly, the recurrence rates of this disease. Targeted medical prophylaxis requires reliable information on stone type which, when combined with relevant blood and urine analyses, allows identification of treatable risk factors. Data from an external quality assurance scheme indicate that stone analysis is poorly performed in many laboratories, and it is probable that this results in ill-informed patterns of investigation, inappropriate therapy, missed diagnoses of rarer causative disorders and wasteful further investigation of 'non-renal' stone artefacts. Renal stone analysis is a specialist investigation requiring appropriate analytical and interpretative expertise if the information is to be used to enhance patient care. For those laboratories not able to offer this, for whatever reason, referral is the only defensible approach to service provision. The methods currently employed in many departments have no place in modern clinical biochemistry practice.

Blood Chemical Analysis↗
PubMed1999

Urinary supersaturation of calcium oxalate and phosphate in patients with X-linked hypophosphatemic rickets and in healthy schoolchildren.

UNLABELLED: Nephrocalcinosis (NC) is a complication of the treatment of X-linked hypophosphatemic rickets (XLHR). Some studies have found that treated patients have enteric hyperoxaluria caused by phosphate therapy and have implicated calcium oxalate, whereas others have found only calcium phosphate in renal biopsy tissue. AIM AND METHODS: We aimed to study the urinary supersaturation of calcium oxalate and calcium phosphate and to determine whether these measures are risk factors for NC. We collected 24-hour urine samples from 20 patients (12 girls) with XLHR, mean +/- SD age 8.2 +/- 4.7 years, and from 79 age-matched members of a healthy control group prospectively. RESULTS: The median 24-hour urine excretions of oxalate, phosphate, and citrate (mmol/1.73 m(2) per day) were significantly increased in patients compared with the control group (oxalate 0.38 vs 0.28, P =. 0012; phosphate 63.1 vs 25.8, P <.0001; citrate 4.18 vs 2.7, P =. 0002). However, no significant differences were seen in the calcium oxalate or calcium phosphate between patients and the control group. No significant differences were seen in 24-hour urine calcium or magnesium excretion between patients and the control group; however, 8 patients had hypercalciuria. A significant higher urine volume in patients compared with the normal group (826 mL/m(2) 24-hour vs 597 mL/m(2) 24-hour; P <.005) was found. Twelve patients had NC at the time of investigation, and although the oxalate excretion was significantly higher in these patients, no significant difference was seen in the relative supersaturation of calcium oxalate monohydrate (CaC(2)O(4).H(2)O) compared with the 8 without NC. CONCLUSIONS: Although 24-hour urine oxalate and phosphate excretion are increased in treated patients with XLHR, there is no increase in the supersaturation of either calcium oxalate or phosphate. Determination of the supersaturation of calcium oxalate or calcium phosphate does not predict the development of NC in XLHR.

Calcium Oxalate↗
PubMed1997

Effects of Tamm-Horsfall protein with normal and reduced sialic acid content upon the crystallization of calcium phosphate and calcium oxalate in human urine.

OBJECTIVE: To examine the effects of Tamm-Horsfall protein (THP) of normal and low sialic acid content on urinary crystallization, and establish whether there are changes conducive to the formation of kidney stones. MATERIALS AND METHODS: Purified samples of THP were recovered from the urine of non-stone forming individuals. A portion of each THP sample was treated with the enzyme neuraminidase to yield the low sialic acid form of the protein. The two forms of THP were added separately to ultrafiltered urine and crystallization was then induced in the urine by evaporation at 37 degrees C. Two types of experiment were then conducted with the crystals that formed; the rate at which the resulting calcium phosphate or calcium oxalate crystals sedimented in the evaporated urine was determined and the proportion of these crystals and protein which was retained when the urine was passed through a 75 microns sieve was measured. RESULTS: Calcium phosphate and calcium oxalate crystals remained in stable colloidal suspension in ultrafiltered urine when in the presence of normal THP; these suspensions passed freely through the 75 microns sieves. When crystals formed in the presence of low sialic acid THP, the sedimentation was rapid and the crystals were readily retained with protein on the sieves. CONCLUSIONS: These results indicate that whilst normal THP inhibits urinary crystal aggregation, the properties of the low sialic acid form are consistent with the promotion of crystal aggregation and hence stone formation.

Calcium Oxalate↗
PubMed1996

The inhibitory activity of some citrate analogues upon calcium crystalluria: observations using an improved urine evaporation technique.

The ability of three compounds, all similar in chemical structure to citric acid, to decrease calcium crystalluria has been measured. The measurements were made in normal human urine at 37 degrees C and compared with the crystal-decreasing power of citric acid when measured in the same way and in the same urine samples. One of the compounds tested, phosphocitric acid, was more potent than citric acid in inhibiting calcium oxalate crystal precipitation. At higher concentrations it also proved more effective against calcium phosphate. A urine evaporation method was used to carry out the crystal inhibition tests after modification to improve its precision.

Calcium Oxalate↗
PubMed1995

Rapid computer-assisted infrared analysis of urinary calculi using photoacoustic detection.

The application of commercial spectrum-analysing software to quantitative analysis of urinary stones by Fourier transform infrared spectrophotometry is described. The infrared technique is straightforward in comparison with other stone analysis procedures of similar scope and affords significant time savings. The use of partial least squares regression in the analysis program enables better quantitation of stone components than has been hitherto possible using infrared methods. All the principal and many less common stone constituents can be detected and measured. Photoacoustic detection was employed, thus enabling non-destructive analysis with minimal sample preparation. A comparison is made between the infrared procedure and the hybrid thermogravimetric plus "wet" chemistry technique, which it has superseded for routine urinary stone analysis in the author's department.

Acoustics↗
PubMed1995

Plasma and urine measurements for monitoring of treatment in the primary hyperoxaluric patient.

Reliable methods for the assaying of oxalate in biological fluids are now available. However, preanalytical sample collection and storage conditions are critical to produce meaningful results for the diagnosis and assessment of treatment modalities in primary hyperoxaluria. Spontaneous in vitro generation of oxalate from ascorbate is possible, especially in plasma measurements, where the ascorbate to oxalate ratio is considerably greater than that of urine. The pH of blood also favours the conversion of ascorbate to oxalate. Losses, as well as generation of oxalate can occur in urine when collection procedures are inadequate. Analysis of properly collected samples is of greater assistance in monitoring the efficacy of treatment modalities in oxaluric patients. Routine and reliable assays are still needed for other closely related organic acid anions such as glycolate and L-glycerate. Measurement of these anions can facilitate the diagnosis and assist in monitoring of treatment in the different forms of primary hyperoxaluria.

Humans↗
PubMed1993

Chemical analysis of post-lithotripsy stone fragments: a critical evaluation.

A scheme for the chemical microanalysis of renal stone fragments recovered from urine voided immediately after lithotripsy has been developed and evaluated. The analytical procedure includes assay of calcium, magnesium, phosphate, oxalate and urate and has been applied to 78 such urine samples. Problems relating to co-existing crystalluria and blood and urine contaminants have been recognised and overcome. However, significant loss of all stone components due to fragment dissolution in urine prior to recovery was found to occur and was investigated. The distribution of stone components found in these analyses was similar to that seen in previous surveys of intact stones.

Calcium↗
PubMed1991

Urinary oxalate and glycolate excretion and plasma oxalate concentration.

The diagnosis of primary hyperoxaluria in young children is hampered by the lack of a reliable reference range for urinary oxalate excretion, especially in infants. We present data on urinary oxalate and glycolate excretion in 137 normal children, on the plasma oxalate concentration in 33 normal children and 53 with chronic renal failure, and on amniotic fluid oxalate concentration in 63 uncomplicated pregnancies. The urinary oxalate:creatinine molar ratios were log normally distributed: mean (range) values were less than 1 year 0.061 (0.015-0.26), 1-5 years 0.036 (0.011-0.12), 5-12 years 0.030 (0.0059-0.15), and greater than 12 years 0.013 (0.0021-0.083). Geometric mean (range) plasma oxalate concentration in the normal children was 1.53 (0.78-3.02) mumols/l and was independent of age. The mean (SD) plasma oxalate: creatinine molar ratio in these normal children and 50 with chronic renal failure was 0.033 (0.013), and was independent of age and renal function. Mean (SD) amniotic fluid oxalate concentration was 19.0 (4.3) mumols/l.

Adolescent↗
PubMed1990

Plasma oxalate and creatinine and oxalate/creatinine clearance ratios in normal subjects and in primary hyperoxaluria. Evidence for renal hyperoxaluria.

Plasma oxalate and creatinine were measured repeatedly in healthy individuals and in 12 patients with type 1 primary hyperoxaluria unresponsive to pyridoxine. The mean ratios were 0.025 (SD 0.006) and 0.120 (SD 0.048), respectively. One patient repeatedly had normal plasma oxalate despite markedly raised urinary oxalate and it seems unlikely that this excess oxalate could have come from the liver. Oxalate/creatinine clearance ratios in the normal group had an overall mean of 0.59 (SD 0.27) in 24 h urine collections and 0.741 (SD 0.297) in repeated short clearance periods. Both renal tubular absorption and secretion of oxalate apparently occurred on different days, but this did not depend upon urinary flow rate. Oxalate/creatinine clearance ratios in type 1 primary hyperoxaluria had a mean of 2.88 (SD 3.11). The raised oxalate/creatinine clearance ratios in the patients were not correlated with either plasma oxalate or creatinine. A few patients showed much higher clearance ratios and in some were sufficiently high to indicate that oxalate was generated and secreted in the kidneys.

Creatinine↗
PubMed1990

Hyperoxaluria or hypercalciuria in nephrolithiasis: the importance of renal tubular functions.

The role of the kidney in states of hyperoxaluria and hypercalciuria was investigated in seven patients with hyperoxaluria after jejunoileal bypass (JIB) and six patients with idiopathic hypercalciuria (IHC). Eight apparently healthy persons formed a control group. Besides hyperoxaluria, the patients with JIB displayed an elevated plasma concentration of oxalate and the oxalate clearance was increased and higher than creatinine clearance, indicating a net tubular secretion of oxalate. The JIB patients had lower 24-h urinary excretions of calcium, phosphate, magnesium and citrate and higher serum parathyroid hormone (PTH) than controls, indicating increased secretion of PTH to compensate for calcium malabsorption. IHC patients exhibited increased fasting urinary calcium even though their serum values were similar to those in the controls. These results indicate a reduced tubular calcium reabsorption, which was most pronounced in patients with highest PTH values. We conclude that hyperoxaluria in JIB patients is associated both with intestinal hyperabsorption and with enhanced tubular secretion of oxalate, and that in some patients with IHC hypercalciuria is due to reduced tubular reabsorption of calcium.

Adult↗
PubMed1989

Failure of allopurinol to modify urinary composition in enteric hyperoxaluria.

Conventional treatment of enteric hyperoxaluria (EHO) consists of dietary restriction of oxalate and fat and correction of its underlying cause whenever possible. Recent work suggests that allopurinol reduces the incidence of urolithiasis and the urinary excretion of both oxalate and uric acid in patients without intestinal disease. We have assessed the effect of allopurinol, 300 mg daily for 2 weeks, on urine biochemistry in patients with EHO due to small bowel Crohn's disease and/or resections. Compliance with treatment was confirmed by a fall in plasma uric acid in every patient. Allopurinol failed to alter 24 h urinary oxalate excretion or oxalate concentration. There were also no significant changes in the urinary excretion of glycollate (like oxalate, a breakdown product of glyoxylate), citrate, magnesium or calcium, each of which was at the lower end of the normal range before and during treatment with allopurinol. It appears unlikely that allopurinol will prove useful in the prevention of urolithiasis in patients with EHO.

Adult↗
PubMed1986

Measurement of plasma oxalate in healthy subjects and in patients with chronic renal failure using immobilised oxalate oxidase.

A continuous flow assay using immobilised oxalate oxidase was used to measure the level of oxalate in plasma ultrafiltrate obtained from healthy subjects and from patients with chronic renal failure. The levels of oxalate in plasma from normal subjects ranged from 1.3-3.1 mumol/l (mean 2.03; SD = 0.52) with females showing a higher (p less than 0.05) level (mean 2.25 mumol/l) than males (mean 1.87 mumol/l). The mean oxalate/creatinine clearance ratio in fourteen healthy subjects was greater than unity, thus indicating a net tubular secretion of oxalate. At physiological pH, L-ascorbate was converted to oxalate in whole blood following venepuncture, in plasma and in plasma ultrafiltrate. Reduction of the spontaneous generation of oxalate in the samples prior to analysis was achieved by acidification and treatment with sodium nitrite. A linear correlation (r = 0.92; p less than 0.001) was found between plasma oxalate and plasma creatinine in patients with chronic renal failure.

Adult↗
PubMed1985

Continuous-flow assay for urinary oxalate using immobilised oxalate oxidase.

A continuous-flow assay for measuring oxalate in urine is described. Covalently attached oxalate oxidase (EC 1.2.3.4) is used to oxidize the oxalate anion to carbon dioxide and hydrogen peroxide. The formed hydrogen peroxide is measured colorimetrically (A580) with an established reaction using horseradish peroxidase (EC 1.11.17), 3-methyl-2-benzothiazolinone hydrazone (MBTH) and 3-dimethylaminobenzoic acid (DMAB). Ascorbate interference is eliminated by treating the urine sample with sodium nitrite prior to assaying. The assay is accurate (mean recovery of added oxalate in spiked urine sample is 93 +/- 11%), sensitive (detection limit 1.0 mumol/L), reproducible (within-batch CV 3.5%; between-batch CV 5%) and relatively rapid (15 samples/h). This assay correlates well (R = 0.99) with another established enzymatic method (using oxalate decarboxylase).

Adolescent↗