Effect of potential renal acid load of foods on urinary citrate excretion in calcium renal stone formers

The aim of this study was to investigate the influence of the potential renal acid load (PRAL) of the diet on the urinary risk factors for renal stone formation. The present series comprises 187 consecutive renal calcium stone patients (114 males, 73 females) who were studied in our stone clinic. Each patient was subjected to an investigation including a 24-h dietary record and 24-h urine sample taken over the same period. Nutrients and calories were calculated by means of food composition tables using a computerized procedure. Daily PRAL was calculated considering the mineral and protein composition of foods, the mean intestinal absorption rate for each nutrient and the metabolism of sulfur-containing amino acids. Sodium, potassium, calcium, magnesium, phosphate, oxalate, urate, citrate, and creatinine levels were measured in the urine. The mean daily PRAL was higher in male than in female patients (24.1±24.0 vs 16.1±20.1 mEq/day, P=0.000). A significantly (P=0.01) negative correlation (R=−0.18) was found between daily PRAL and daily urinary citrate, but no correlation between PRAL and urinary calcium, oxalate, and urate was shown. Daily urinary calcium (R=0.186, P=0.011) and uric acid (R=0.157, P=0.033) were significantly related to the dietary intake of protein. Daily urinary citrate was significantly related to the intakes of copper (R=0.178, P=0.015), riboflavin (R=0.20, P=0.006), piridoxine (R=0.169, P=0.021) and biotin (R=0.196, P=0.007). The regression analysis by stepwise selection confirmed the significant negative correlation between PRAL and urinary citrate (P=0.002) and the significant positive correlation between riboflavin and urinary citrate (P=0.000). Urinary citrate excretion of renal stone formers (RSFs) is highly dependant from dietary acid load. The computation of the renal acid load is advisable to investigate the role of diet in the pathogenesis of calcium stone disease and it is also a useful tool to evaluate the lithogenic potential of the diet of the individual patient.     

Renal tubular acidosis: Effects of etacrynic acid on renal acid and calcium excretion

Summary The fundamental disorder in renal tubular acidosis —the impaired excretion of hydrogen ions — can favourably be influenced by etacrynic acid (Hydromedin^®). Net acid and calcium excretion was measured in eight patients with incomplete RTA I and five controls before and during treatment with the diuretic: urinary pH was lowered and net acid excretion increased (p<0.05) with only slight rise in urinary calcium. Etacrynic acid appears to be particularly suitable for the long term treatment of patients with incomplete RTA I and calculous disease.     

Renal function in children with idiopathic hypercalciuria

Abnormalities in renal tubular function have been reported in adult patients with idiopathic renal hypercalciuria. To determine if such abnormalities are present early in the natural history of renal hypercalciuria, we evaluated renal tubular function in ten children with idiopathic renal hypercalciuria, aged 5–17 years. Seven of the children presented with urolithiasis and three with hematuria. Urinary calcium excretion ranged from 4 to 9 mg/kg per day, (5.2±0.5, mean ± SEM) with a mean fasting urinary calcium to creatinine ratio of 0.31±0.03. Studies described in this report were performed after 1 week of ingesting a diet containing 1,000 mg calcium, 3,000 mg sodium, and 100 mg purine. Clearance of creatinine ranged from 84 to 159 ml/min per 1.73 m². Tm phosphate (mg/100 ml GFR) was normal in each child (mean 4.66±0.06 mg/100 ml GFR). Fractional excretion of uric acid, sodium and beta-2-microglobulin were also normal in each child. Serum bicarbonate concentrations ranged from 21.5 to 27 mEq/l with a mean of 24.4±0.5 mEq/l and all patients lowered urinary pH to <5.5. Hypotonic diuresis demonstrated normal free water clearance with a mean of 12.8 ml/min per 100 ml C_in. Distal sodium delivery and fractional distal sodium reabsorption were normal with a mean of 13.6±1.2% and 92.7±0.5%, respectively. Water deprivation studies demonstrated a range of maximum urinary osmolality from 711 to 1,020 mosmol/kg H₂O with a mean of 864±34 mosmol/kg H₂O. Seven healthy children, ingesting an identical study diet, concentrated their urine to a mean of 1,059±31 mosmol/kg h₂O. Thus, only a partial defect in urinary concentrating ability was identified in these studies of renal function in children with renal hypercalciuria. Our data demonstrate that idiopathic renal hypercalciuria is not the result of a generalized renal tubulopathy nor is it the result of renal tubular acidosis in these children. These findings suggest that renal tubular dysfunction in adult patients with hypercalciuria may be secondary to repeated episodes of urolithiasis or to life-long hypercalciuria.This project was supported by a Clinical Associate Physician Award (FBS) no. RR00211-19 from the General Clinical Research Center     

Renal net acid excretion related to body surface area in children and adolescents

Renal net acid excretion (NAE) was determined in 2307 24-h urine samples from 566 healthy children and adolescents (285 boys, 281 girls; 2.7–18.3 years) participating in the DONALD (Dortmund Nutritional and Anthropometric Longitudinally Designed) Study. NAE is presented for 32 different age and sex groups. Before puberty there is an age-dependent increase in absolute values of NAE (mmol/day) and an age-dependent decrease in NAE related to body weight (mmol/kg per day). NAE related to body surface area (mmol/day per 1.73 m²) was independent of age with higher values in boys than in girls. In summary, body surface area is an appropriate adjustment parameter for renal NAE in the age-independent assessment of the renal acid load in German children and adolescents. Received: 12 November 1999 / Revised: 15 March 2000 / Accepted: 17 April 2000     

Renal tubular acidosis and osteopetrosis with carbonic anhydrase II deficiency: pathogenesis of impaired acidification

Renal tubular acidosis with osteopetrosis is an autosomal recessive disorder due to deficiency of carbonic anhydrase II (CAII). A 3.5-year-old Egyptian boy with osteopetrosis and cerebral calcification had a persistent normal anion gap type of metabolic acidosis (plasma pH 7.26) and a mild degree of hypokalemia. A baseline urine pH was 7.0; ammonium (NH₄ ⁺) excretion was low at 11 μmol/min per 1.73 m²; fractional excretion of bicarbonate HCO₃ (FE_HCO3) was high at 9%, when plasma HCO₃ was 20 mmol/l; citrate excretion rate was high for the degree of acidosis at 0.35 mmol/mmol creatinine. Intravenous administration of sodium bicarbonate led to a urine pH of 7.6, a FE_HCO3 of 14%, a urine-blood PCO₂ difference of 7 mmHg, NH₄ ⁺ excretion fell to close to nil, and citrate excretion remained at 0.38 mmol/mmol creatinine. Intravenous administration of arginine hydrochloride caused the urine pH to fall to 5.8, the FE_HCO3 to fall to 0, the NH₄ ⁺ excretion rate to rise to 43 μmol/min per 1.73 m², and citrate excretion to fall to <0.01 mmol/mmol creatinine. These results show that our patient had a low rate of NH₄ ⁺ excretion, a low urine minus blood PCO₂ difference in alkaline urine, and a low urinary citrate excretion, but only when he was severely acidotic. He failed to achieve a maximally low urine pH. These findings indicate that his renal acidification mechanisms were impaired in both the proximal and distal tubule, the result of his CA_II deficiency. Received October 24, 1996; received in revised form and accepted February 20, 1997     

Evaluation of lithogenic elements in urine of healthy newborns

The determination of urinary excretion of lithogenic elements in healthy newborns involves factors ranging from urine collection and data handling to maternal influences, which can cause difficulties in analyzing the results. The objective of this study was to determine normal values of parameters related to lithogenesis, such as calcium, uric acid, citrate, and oxalate, in urine of healthy newborns using isolated samples, focusing on variations according to gender, weight, milk ingestion, and family history of lithiasis. Parameters measured in isolated urine samples from 104 healthy newborns (77 males and 27 females) were corrected by creatinine. The ratios were expressed as milligram/milligram of creatinine: calcium/creatinine of 0.10±0.01 (X±SE), uric acid/ creatinine of 1.10±0.10, citrate/creatinine of 0.56±0.04, and oxalate/creatinine of 0.07±0.01. Differences were observed between males and females, in terms of uric acid (0.80±0.07 vs. 1.10±0.10 mg/mg, P<0.05), citrate (0.05±0.06 vs. 0.17±0.05, P<0.05), sodium (0.17± 0.01 vs. 0.05±0.01, P<0.001), and potassium (0.05± 0.01 vs. 0.20±0.02, P<0.001). Interestingly, the urinary concentration of protector factors such citrate and potassium was higher in females than in males with low sodium excretion. Artificial milk feeding leads to higher calcium (0.10±0.06 vs. 0.06±0.01), uric acid (1.40±0.20 vs. 0.90±0.09, P<0.05), citrate (0.90±0.09 vs. 0.50±0.04, P<0.001), and oxalate (0.17±0.03 vs. 0.05±0.01, P<0.001) excretion when compared with breast feeding. There was higher excretion of calcium and sodium in patients under 3 kg. Children with familial antecedents presented some differences in urinary excretion, with higher uric acid (1.50±0.30 vs. 0.80±0.08, P<0.05) but lower calcium (0.05±0.02 vs. 0.10±0.01, P<0.05) and sodium (0.15±0.02 vs. 0.20±0.02, P<0.05) excretion, respectively. This report provides urinary parameters obtained in healthy newborns and correlates them with factors that could be involved in the genesis of osteopenia, renal stones, and/or nephrocalcinosis. Received: 8 May 2000 / Revised: 7 June 2001 / Accepted: 12 June 2001     

Urinary aquaporin-2 in children with acute pyelonephritis

Children with acute pyelonephritis develop polyuria and have reduced maximum urinary concentration capacity. We studied whether these abnormalities are associated with altered urinary excretion of the water channel aquaporin-2 (AQP2) in the renal collecting duct. AQP2 is the main target for antidiuretic action of arginine vasopressin (AVP), and the urinary excretion of this protein is believed to be an index of AVP signaling activity in the kidney. Children with acute pyelonephritis, aged 5–14 years, were examined for urinary flow rate, creatinine clearance, unchallenged urine osmolality, and urinary ion excretion. Urinary excretion of AQP2 was measured by dot immunoblotting technique. Studies were performed in the acute phase of pyelonephritis, in the same children after treatment, and in control patients. At the onset of pyelonephritis, urinary flow rate and solute excretion were increased, but the urinary osmolality was unchanged. The urinary level and urinary excretion of AQP2 was increased in acute pyelonephritis and decreased after treatment. Excretion of aquaporin-3 was unchanged, suggesting that the increase in AQP2 urinary excretion was not due to a shedding of collecting duct cells. The results suggest that a mechanism proximal to the collecting duct may be responsible for the polyuria observed in children with acute pyelonephritis. Increased urinary AQP2 levels suggest that a compensatory activation of apical plasma membrane targeting of AQP2 may occur in pyelonephritis.     

Renal tubular acidosis (RTA):RecognizeTheAmmonium defect and pHorget the urine pH

To maintain acid-base balance, the kidney must generate new bicarbonate by metabolizing glutamine and excreting ammonium (NH₄ ⁺). During chronic metabolic acidosis, the kidney should respond by increasing the rate of excretion of NH₄ ⁺ to 200–300 mmol/day. If the rate of excretion of NH₄ ⁺ is much lower, the kidney is responsible for causing or perpetuating the chronic metabolic acidosis. Thus, the first step in the assessment of hyperchloraemic metabolic acidosis is to evaluate the rate of excretion of NH₄ ⁺. It is important to recognize that the urine pH may be misleading when initially assessing the cause of this acidosis, as it does not necessarily reflect the rate of excretion of NH₄ ⁺. If proximal renal tubular acidosis (RTA) is excluded, low NH₄ ⁺ excretion disease may be broadly classified into problems of NH₄ ⁺ production and problems of NH₄ ⁺ transfer to the urine; the latter being due to either interstitial disease or disorders of hydrogen ion secretion. The measurement of the urine pH at this stage may identify which problem predominates. This approach returns the focus of the investigation of RTA from urine pH to urine NH₄ ⁺.     

Distal renal tubular acidosis: the value of urinary pH,PCO2 and NH4 + measurements

Distal renal tubular acidosis (dRTA) is not a single disease. The experimental forms of the syndrome are unsatisfactory as models of the naturally occurring disease, not least because they are seldom complicated by nephrocalcinosis, which is present in the majority of patients with spontaneous disease and contributes to the renal tubular defects found in the syndrome. Impairment of minimal urine pH, reduced urine carbon dioxide tension (PCO₂) during passage of alkaline urine, and reduced urinary ammonium (NH₄ ⁺) excretion, have all been advocated as essential criteria for the diagnosis of dRTA. Minimal urine pH, measured during metabolic acidosis, sulphate infusion, or after oral frusemide, is the yardstick against which other criteria should be assessed. A reduced urinaryPCO₂ is commonly found in dRTA but is not specific for the syndrome and may be accounted for by tubular defects other than those involving reduced distal hydrogen ion secretion. NH₄ ⁺ excretion is reduced in most patients with renal acidosis whatever the nature of the underlying renal disease; this function is closely related to nephron mass, and is not specifically impaired in renal tubular disease.     

Renal tubular dysfunction in fetal alcohol syndrome

Renal function was evaluated in six patients with fetal alcohol syndrome (FAS) and eight control subjects before and after fluid restriction and acute acid loading. Baseline serum electrolytes, creatinine clearance, fractional sodium excretion, tubular reabsorption of phosphate, urine and blood pH and osmolalities, plasma renin activity, and plasma aldosterone level were normal in all subjects, but fractional potassium excretion (FE_K) was lower in FAS patients than in control subjects (P<0.001). Despita equivalent plasma osmolalities (295±3 vs 293±2 mosmol/kg,P=0.2), the maximum urinary osmolality after 12 h of water deprivation in patients with FAS was significantly lower compared with controls (560±107 vs 965±77 mosmol/kg;P<0.001) and increased to only 578±101 mosmol/kg after vasopressin administration. After ammonium chloride loading, minimum urine pH was significantly higher in patients than in controls (5.7±0.17 vs 4.81±0.19;P<0.001). Net acid excretion and FE_K were also lower in patients than in controls (102±11 vs 139.6±11.3 Eq/min per 1.73 m² and 23.5±1.3 vs 29±1.6%, respectively;P<0.001). The data indicate a subclinical renal tubular defect in urine concentration and acidification in patients with FAS.     

The differential diagnostic value of urinary enzyme and amino acid excretion in children with nephrotic syndrome

Urinary enzymesN-acetyl--d-glucosaminidase (NAG) and -glutamyl transpeptidase (-GT) are sensitive markers of specific renal cell damage. Excessive urinary amino acid excretion may also be an indicator of renal tubular damage. We have evaluated urinary excretion of NAG,-GT and 37 amino acids, phospholipids and dipeptides in 30 children (aged 2.3–18.1 years) with nephrotic syndrome (NS), 23 with minimal change nephrotic syndrome (MCNS), 7 with focal segmental glomerulosclerosis (FSGS) and 16 healthy age-matched controls. Nine MCNS patients were in relapse and 14 in remission. Enzyme activity is expressed as micromoles per milligram urinary creatinine. In FSGS, NAG excretion correlated with the following: blood urea nitrogen (BUN) (r=0.8), serum protein (r=0.57), serum cholesterol (r=0.85), serum albumin (r=–0.68) and proteinuria (r=0.56). In FSGS the -GT excretion was not significantly different from MCNS in remission or in relapse. In FSGS, -GT excretion correlated with the following: BUN (r=0.48), serum creatinine (r=–0.66), serum protein (r=–0.54), serum albumin (r=–0.68) and serum cholesterol (r=0.87). Compared with controls, the urinary excretion of 5 amino acids was increased in FSGS patients as a possible indicator of tubular damage. The value for 7 amino acids was reduced in MCNS patients. Urinary amino acid excretion was not different from controls for the other amino acids in either FSGS or MCNS. These data suggest that urinary enzyme excretion, particularly NAG excretion, and amino acid excretion may be useful in the diagnosis and degree of disease in these histological forms of NS in children.Crippled Childrens Foundation Research Center     

Clinical and biochemical profile of patients with “pure” uric acid nephrolithiasis compared with “pure” calcium oxalate stone formers

The purpose of the present study was to compare the clinical characteristics of “pure” uric acid (UA) stone formers with that of “pure” calcium oxalate (CaOx) stone formers and to determine whether renal handling of UA, urinary pH, and urinary excretion of promoters and inhibitors of stone formation were different between the two groups. Study subjects comprised 59 patients identified by records of stone analysis: 30 of them had “pure” UA stones and 29 had “pure” CaOx nephrolithiasis. Both groups underwent full outpatient evaluation of stone risk analysis that included renal handling of UA and urinary pH. Compared to CaOx stone formers, UA stone formers were older (53.3 ± 11.8 years vs. 44.5 ± 10.0 years; P = 0.003); they had higher mean weight (88.6 ± 12.5 kg vs. 78.0 ± 11.0 kg; P = 0.001) and body mass index (29.5 ± 4.2 kg/m² vs. 26.3 ± 3.5 kg/m²; P = 0.002) with a greater proportion of obese subjects (43.3% vs. 16.1%; P = 0.01). Patients with “pure” UA lithiasis had significantly lower UA clearance, UA fractional excretion, and UA/creatinine ratio, with significantly higher serum UA. The mean urinary pH was significantly lower in UA stone formers compared to CaOx stone formers (5.17 ± 0.20 vs. 5.93 ± 0.42; P < 0.0001). Patients with CaOx stones were a decade younger, having higher 24-h urinary calcium excretion (218.5 ± 56.3 mg/24 h vs. 181.3 ± 57.1 mg/24 h; P = 0.01) and a higher activity product index for CaOx [AP (CaOx) index]. Overweight/obesity and older age associated with low urine pH were the principal characteristic of “pure” UA stone formers. Impairment in urate excretion associated with increased serum UA was also another characteristic of UA stone formers that resembles patients with primary gout. Patients with pure CaOx stones were younger; they had a low proportion of obese subjects, a higher urinary calcium excretion, and a higher AP index for CaOx.     

Renal function in pediatric patients with β-thalassemia major

In patients with β-thalassemia major, the most important cause of mortality and morbidity is organ failure due to deposits of iron.. In this study, the nature of the kidney injury and possible pathogenetic factors were investigated. Seventy children with β-thalassemia major and 14 age and sex-matched healthy children were involved in the study. Blood and timed urine samples were obtained for hematological and biochemical tests. The mean values of blood urea nitrogen (BUN), serum creatinine, creatinine clearance, serum sodium, urine osmolality, fractional excretion of sodium, potassium, and uric acid were not statistically different between the groups. Serum levels of potassium, phosphorus, and uric acid and the urine volume, high urinary protein to creatinine (U_P/Cr), urinary N-acetyl-β-d-glucosaminidase to creatinine (U_NAG/Cr), and urinary malondialdehyde to creatinine, (U_MDA/Cr) and the tubular phosphate reabsorption (TRP) values were statistically different between two groups (P<0.05). Increased serum levels of potassium, phosphorus, and uric acid in the patient group were attributed to the rapid erythrocyte turnover. The presence of high U_P/Cr, U_NAG/Cr and U_MDA/Cr ratios shows that in these patients with proximal renal tubular damage may be secondary to oxidative lipid peroxidation mediated by the iron overload. Received: 30 September 1999 / Revised: 19 May 2000 / Accepted: 22 May 2000     

Protein intake can not be estimated from urinary urea excretion

We assessed the relationship between protein intake (calculated from a 3-day prospective dietary diary) and 24-h urinary urea excretion in 37 children with chronic renal failure. Protein intake was not restricted during the investigation period. The 24-h urinary urea excretion correlated poorly with the protein intake estimated from the dietary diary (r=0.58). We conclude that although it is common practice to assess compliance with a protein-restricted diet in children with chronic renal failure with a dietary diary and 24-h urinary urea excretion, the value of this assessment is questionable.     

Furosemide-Induced Increase in Urinary and Peritoneal Excretion of Uric Acid During Peritoneal Dialysis in Patients with Chronic Uremia

Intermittent peritoneal dialysis was performed in 17 patients with chronic uremia in order to observe the effect of furo-semide added to the dialysate on urinary and peritoneal elimination of uric acid. Two kinds of dialysate were used: moderately hypertonic (osmolality, 431.2 mOsm/kg of water) and slightly hypertonic (osmolality, 368.9 Osm/kg of water). Significant increases in urine volume, urinary and peritoneal excretion of uric acid, and renal and peritoneal clearances were found. The increase in urinary excretion of uric acid exceeded that of urine volume. These findings were interpreted to be the result of furosemide action on renal function after being transferred through the peritoneum into the blood stream with the concomitant increase in the uric acid shift from the circulation into the peritoneal cavity. We concluded that the addition of furosemide is useful in increasing uric acid elimination in patients with chronic uremia.     

Primary role of hyperkalemia in the acidosis of hyporeninemic hypoaldosteronism

A 65-year-old woman with mild renal insufficiency had persistent hyperkalemia and hyperchloremic acidosis. Her plasma aldosterone level was relatively low for her hyperkalemia, and her urine pH was low. Fludrocortisone acetate administration corrected both hyperkalemia and acidosis by increasing urinary excretion of potassium and net acid, implicating deficient mineralocorticoid activity in the distal renal tubule in this patient. During this medication urinary ammonium excretion increased, but urine pH remained low, so that urinary titratable acid excretion did not decrease. On the other hand, correction of hyperkalemia by administration of a potassium-calcium exchange resin alone also resolved the acidosis by increasing urinary ammonium excretion. This increment exceeded the decrement of urinary titratable acid excretion, which was caused by raised urine pH secondary to increased urinary ammonium excretion, and resulted in increase of net acid excretion. Thus, in this patient, hyperkalemia appears to be a decisive causative factor in the acidosis, with deficient mineralocorticoid effect only contributing in part to the reduction of net acid excretion and the acidosis.     

Quantification of proteinuria in children using the urinary protein-osmolality ratio

A prospective study was conducted to determine the correlation of early morning urinary protein/osmolality ratio (mg/l/mosmol/kg) with 24-h urinary protein excretion (mg/m²/day). Study patients consisted of 53 children (aged 1 month to 15 years). Early morning urine samples and 24-h urine samples were collected and analyzed. In group 1 (children without proteinuria), early morning urinary protein/creatinine ratio (Uprot/Ucr, mg/mg) was 0.061±0.011 and the protein/osmolality ratio (Uprot/Uosm, mg/l/mosmol/kg) was 0.073±0.014. Twenty-four hour urinary protein excretion in group 1 had no significant correlation with Uprot/Ucr or Uprot/Uosm. In group II (children with proteinuria), Uprot/Ucr was 5.78±1.10 and Uprot/Uosm was 4.42±1.34. Twenty- four hour urinary protein excretion in group 2 was 1483.6±303.7 mg/m²/day and its correlation with both Uprot/Uosm and Uprot/Ucr was highly significant (r= 0.87, P<0.001 and r=0.88, P<0.001, respectively). The accepted nephrotic level of proteinuria of 40 mg/m²/h coincides with a Uprot/Uosm ratio of 1.9. In conclusion, early morning urinary Uprot/Uosm is a simple and potentially useful test for 24-h urinary protein excretion, and possibly could be used safely for the assessment of the degree of proteinuria in children. Received: 13 April 1999 / Revised: 23 February 2000 / Accepted: 15 August 2000     

Urinary mineral excretion among normal Taiwanese children

Prompted by a large population of children with renal stones seen in 20 of our country's teaching hospitals over the past 10 years, this study of urinary mineral excretion in normal children was performed. Fasting urine from 1,072 normal Taiwanese school children and 24-h urine collections from 125 children separated into three age groups were analysed for calcium (Ca), phosphate, magnesium (Mg), uric acid, sodium (Na) and creatinine (Cr). Fasting Ca/Cr ratios were not different between the sexes. Ca/Cr ratios were higher in the 17- to 18-year age group as were 24-h urinary Ca excretions. Urinary Mg/Cr ratios were higher in girls than boys and 24-h urinary Mg excretion was highest in the younger age groups. Urinary Mg excretion in Taiwanese children is 54%–86% lower than previously reported in Caucasian children. Both uric acid/Cr ratios and 24-h urinary uric acid excretion were highest in the youngest children. Urinary Na/Cr ratios and 24-h urinary Na excretion were higher in the two younger age groups. There was no correlation between 24-h urinary Ca and Na excretion.     

Litiasis en pediatría: correlación de métodos que dependen de la recogida de orina de 24 horas con otros más sencillos que no requieren orina minutada

IntroductionDaily practice requires quick, simple and accessible methods to appropriately assess the urinary excretion of solutes in diagnostic or follow-up evaluations of children with renal lithiasis.ObjectivesThe objective of this study was to correlate urine elimination of substances related to renal lithiasis that depend on the volume of excreted urine in a unit of time with other parameters that are calculated by measuring the concentration of these substances in blood and urine, such as urinary ratios, fractional excretions and excretion rates.Materials and methodsThe study included 401 healthy children aged 3-14 years (187 boys and 214 girls), mean age 8.78±3.40 years. The analysis was carried out by Pearson's correlation coefficient.ResultsThere was significant correlation between the elimination of sodium, potassium and chlorine in 24-hour urine sample and the urinary ratios and fractional excretions of these ions.Urinary ratios and rates of excretion of calcium, uric acid, phosphate, magnesium, citrate and oxalate were highly correlated with the determinations of these substances in 24-hour collections.ConclusionsThese equations provide relevant information for the study of the etiology of renal lithiasis in children, as well as about compliance to dietary treatment. They also assess the effectiveness of the various treatments used in these patients, without having to resort to 24-hour collections, which pose a considerable challenge in the pediatric age group.     

Abnormal urinary acidification in infants with hydronephrosis

 Distal renal tubular abnormalities have been observed in patients with dilated urinary tract disorders. The present study was undertaken to look for patterns in urinary acidification in infants with varying degrees of hydronephrosis due to either reflux or obstruction and occurring as unilateral or bilateral disease. Three groups of infants (mean age 3.7±3.8 months) were studied prospectively. Groups IA and IB included patients with hydronephrosis who were acidotic and non-acidotic, respectively. Group II served as controls and consisted of patients with diarrhea and secondary metabolic acidosis with no known renal disease. Serum electrolytes, creatinine, and urine pH were measured in all patients. Urinary titratable acidity, ammonium (NH₄), and net acid excretion (NAE) were measured by the titrimetric method. Infants with hydronephrosis demonstrated lower urinary buffering capacity, reflected in low NAE in the face of acidosis. Deficiencies were noted in both titratable acid and NH₄ excretion compared with control infants. Acidosis was as common in unilateral as in bilateral disease, regardless of severity score. These data confirm a defect in distal urinary acidification in infants with hydronephrosis, whether unilateral or bilateral. Immaturity and endogenous acid load may play a significant role in the manifestation of metabolic acidosis with unilateral disease. Received: 3 June 1997 / Revised: 7 July 1998 / Accepted: 8 July 1998