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Maximum tubular reabsorptive capacity

F. The maximum tubular reabsorptive capacity for phosphate (Tmp) can be determined by a more elaborate phosphate infusion procedure (A3, T8). The normal range is reported as 1.4. 9mg/min (R6). It has frequently been shown that the Tmp is not reduced in primary hyperparathyroidism (T8, R6). [Pg.297]

Azotaemia develops progressively with an increase in creatinine and urea. These findings point to a drop in the glomerular filtration rate (GFR) and renal blood flow. The quotient of creatinine in the urine and plasma is high (>40). Likewise, the quotient of urea-N in the urine and plasma is elevated (> 8). There is a reduction in creatinine clearance within 24 hours to < 40 ml/min. The serum value of urea displays a disproportionate increase compared to creatinine (urea-N/creatinine ratio >20), since the tubular reabsorptive capacity with respect to urea depends on diuresis (maximum 2 ml/ min). In hepatorenal syndrome, the minimal urinary flow gives rise to a longer tubular period of contact with greater tubular reabsorption of urea. [Pg.326]

Polyuria is a recognized clinical feature of primary hyperparathyroidism (CIO). It has been shown to be associated with a reduction in maximum tubular water reabsorptive capacity which cannot be explained by general impairment of renal function and which has been found to improve after parathyroidectomy, as shown in Table 6 (R8). Hellstrom (H4) has found that it is unusual for a case of primary hyperparathyroid-... [Pg.304]

Specific defects in particular functions of the nephrons can also be identified and evaluated. For example, assessment of the maximum concentrating capacity of the kidneys gives an estimate of antidiuretic hormone (ADH)-controUed reabsorption of solute-free water in the distal portion of the tubule. Pinpoint defects, caused by genetically determined deficiencies of specific tubular transport systems or ion channels and giving rise to characteristic biochemical disorders, are considered in Chapter 45. [Pg.797]


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