To address whether a renal tubular dysfunction is encountered in a particular patient subgroup with urolithiasis, the following parameters of tubular function were measured in urine taken in the morning from 214 stone formers after fasting: pH, excretion of lysozyme and gamma-glutamyl transferase (gamma-GT); fractional excretion (FE) of glucose, insulin, Mg, K, and HCO3 after an alkali loading; and the renal threshold for phosphate (TmP/GFR). The following diagnoses were made in the patient group: primary hyperparathyroidism (N = 8), medullary sponge kidneys (N = 21), hyperuricemia (N = 10), cystinuria (N = 2), struvite stone disease (N = 6), idiopathic hypercalciuria of the absorptive (N = 25), dietary (N = 69) or renal (N = 7) type, and normocalciuric idiopathic urolithiasis (N = 66). In 31% of the patients TmP/GFR was below 0.80 mmole/liter and in 13% of the patients, FE HCO3 after alkali loading was above normal. Urinary excretion of lysozyme and that of gamma-GT both were elevated in 17% of the patients. FE glucose, FE insulin, FE Mg, and FE K were elevated in 8, 9, 3, and 7% of the patients, respectively. This study demonstrates that a significant number of stone formers present with signs of renal tubular dysfunction, primarily involving the proximal tubule since apparent leaks of phosphate and of bicarbonate were most frequently encountered. The defects were not specific for a given etiologic group of patients; on the other hand, occurrence was related to the presence of large stones in the pyelocaliceal system at the time data were gathered. Taken together these data suggest that the tubulopathy in nephrolithiasis is the consequence rather than the cause of the stone.

Urinary oxalate excretion was measured in 101 male idiopathic calcium (Ca) stone formers studied on 3 dietary conditions (free-choice, Ca-enriched, and low-Ca diet). The population consisted of 38 normocalciuric and 63 hypercalciuric patients. Mean oxalate excretion was similar in normocalciuric and in hypercalciuric patients, on free-choice as well as on Ca-enriched diet. In both conditions the incidence of hyperoxaluria ( ≥ 435 μmol/24 h) within each group of stone formers was also similar, ranging from 11 to 22%. On low-Ca diet, however, mean oxalate excretion increased significantly (p < 0.01) in hypercalciurics but not in normocalciurics; on this diet, the incidence of hyperoxaluria was particularly high in the hypercalciurics (33%), compared with the normocalciurics (13%). On low-Ca diet, oxalate excretion was positively correlated with the estimated degree of intestinal absorption of calcium (p=0.01). These results show that among idiopathic stone formers, mild hyperoxaluria is not a rare finding and that this disorder can be encountered in each group of patients; its incidence, however, is influenced by the calcium content of the diet. On a low-Ca diet, patients with intestinal Ca hyperabsorption are particularly prone to develop hyperoxaluria, an observation which leads to question the relevance of such a dietary advice unless oxalate intake is simultaneously reduced.

Immunoreactive parathyroid hormone (PTH) levels and nephrogenous cyclic adenosine monophosphate (cAMP) have been reported to be useful parameters in the diagnosis of hyperparathyroidism. Measurements in hyperparathyroid patients usually give values above the normal range when PTH is measured with a carboxyterminal radioimmunoassay and when nephrogenous cAMP is related to glomerular filtration rate. We tested these two parameters in two groups of hypercalcaemic patients (twelve cases of primary hyperparathyroidism and fourteen cases of hypercalcaemia of non-parathyroid origin) and in two groups of normocalcaemic subjects (twenty-one young healthy volunteers and fourteen elderly subjects without parathyroid disease). Slight impairment of renal function caused elevated values of immunoreactive parathyroid hormone in a carboxyterminal radioimmunoassay and also of nephrogenous cAMP when related to glomerular filtration rate. We found that elevated nephrogenous cAMP without parathyroid disease could be attributed to renal insufficiency and to the mode of expression generally used for the nephrogenous cAMP.