Study on Acid-Base Balance Disorders and the Relationship Between Its Parameters and Creatinine Clearance in Patients with Chronic Renal Failure

Due to reduced scope of renal function in chronic renal failure (CRF) it is not rare that it comes to marked metabolic acidosis and pathologic catabolism associated with hypoxia. The cause of metabolic acidosis is deminished tubular secretion of ammonia, due to reduced synthesis, stipulated by lower number of renal canaliculi. Acid-base balance was analyzed in 74 patients suffering from CRF who were on haemodialysis program. Heparinised blood was taken from these patients before and after haemodialysis in which the following parameters were measured: pH, pCO2, pO2, HCO-3 ?, TCO2. The aim of this study was the monitoring of patients' acid-base status before and after haemodilalysis in order to evaluate the degree of stabilization of acid-base balance after haemodilalysis and also to define the correlation between the etiology of CRF and the degree of acid-base balance disorder. In relation to underlying disease resulting in CRF, the patients were divided into five groups: I-tubular interstitial nephrosis (TIN), II-polycystic kidney disease (ADPKD), III-glomerulonephritis (GN), IVhypertension and nephroangio-sclerosis (HTA-Nascl) and V-consisting of patients whose underlying disease was not diagnosed (ERSD). The obtained values of pH, HCO2 and TCO2 after haemodialysis (pH = 7.428 ? 0.06; HCO-3 ?= 25.4 ? 3.44 mmol/L; TCO2 = 26.57 ? 3.56 mmol/L), were significantly increased (p<0.001), in relation to values before haemodialysis (pH = 7.350 ? 0.05; HCO-3 ?= 20.88 ? 2.92 mmol/L; TCO2 = 22.03 ? 3.00 mmol/L). There was no statistically significant difference in values of measured parameters (p>0.05) in relation to underlying disease either before or after haemodialysis both in males and females.

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Effect of an acute oral protein load on renal acidification in healthy humans and in patients with chronic renal failure.

Journal of the American Society of Nephrology ◽

10.1681/asn.v85784 ◽

1997 ◽

Vol 8 (5) ◽

pp. 784-792

Author(s):

N G de Santo ◽

G Capasso ◽

G Malnic ◽

P Anastasio ◽

L Spitali ◽

...

Keyword(s):

Renal Failure ◽

Metabolic Acidosis ◽

Chronic Renal Failure ◽

Urinary Excretion ◽

Healthy Subjects ◽

Tubular Reabsorption ◽

Renal Tubules ◽

Acid Base Balance ◽

Acid Base ◽

Base Balance

The effect of a meat load on the renal handling of acid-base balance was studied in ten healthy subjects (GFR by inulin clearance = 98.5 +/- 8.14 ml.min-1.1.73 m-2) and in ten patients affected by chronic renal failure (CRF) (GFR = 39.9 +/- 5.3 ml.min-1.1.73 m-2). After the meat load (2 g.kg-1 body weight of cooked unsalted red meat), GFR increased by 26.9% (peak value) over baseline in healthy subjects and by 32% in CRF patients. The acid-base status of the healthy subjects was in the normal range, whereas the CRF patients disclosed a slight metabolic acidosis. After a meat load, there was, in the healthy subjects, an increase in the filtered load of bicarbonate coupled to an enhanced tubular reabsorption and urinary excretion. The time course between bicarbonate load and urinary excretion was coincident. In CRF patients, the increase of bicarbonate tubular load after the meal was associated with an increase in tubular reabsorption but not in urinary excretion of this anion. The relationship between bicarbonate load and reabsorption was linear in both groups up to the highest filtered loads. Baseline titratable acidity (TA) and ammonium (NH4+) excretion (expressed per ml GFR) were increased in CRF patients as compared with control subjects, but no changes were found after the meat load in both groups in these experimental conditions. The data indicate that the renal tubules contribute to the maintenance of acid-base balance both in healthy subjects and in CRF patients by reabsorbing most of the additional bicarbonate load. The transient, but significant, increase in bicarbonate excretion observed in healthy subjects could be related to the increased tubular load of bicarbonate. In CRF patients, tubular bicarbonate reabsorption was more complete, possibly because of the stimulation of H+ secretion by the mild metabolic acidosis. TA and NH4+ did not participate in tubular compensation of the increased buffer load.

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