Water-electrolyte disorders in chronic kidney disease of "nonglomerular" etiology

BACKGROUND. The kidneys play a key role in maintaining water-electrolyte homeostasis. However, for the diagnosis of chronic kidney disease (CKD), only indicators reflecting the degree of damage to the glomeruli are used. Electrolyte transport disorders that are directly related to maintaining circulating blood volume, blood pressure, osmotic pressure, and acid-base status are not taken into account. The aim of the study was to clarify the role of water-electrolyte disorders in "non-glomerular" kidney diseases. PATIENTS AND METHODS. 145 patients with CKD of "nonglomerular" etiology aged 50.2±13.9 years were examined, among them 76 men and 69 women. The causes of CKD were chronic tubulointerstitial nephritis (CTIN, 31 patients), type 2 diabetes mellitus (DM, 33 patients), hypertension (AH, 45 patients), AL-amyloidosis (AL, 36 patients). A traditional nephrological clinical and laboratory examination was performed, including determination of concentrations of creatinine, urea and electrolytes in blood serum and urine. Based on the data obtained, urinary clearance and excreted fractions of each of these substances were calculated according to standard algorithms, as well as proximal and distal sodium reabsorption. Statistical analysis of the obtained data was carried out using generally accepted parametric and nonparametric methods. RESULTS. The main indicators in the examination of patients corresponded to the clinical picture of the nature of kidney damage in the underlying disease. Patients of all groups consumed 30-60 % of dietary protein, and table salt was 1.9-2.2 times higher than recommended standards. The proximal sodium reabsorption was 15-25  % higher than normal values. Salt intake positively correlated with urinary clearance of creatinine, urea; potassium; sodium; calcium; chlorine; inorganic phosphate; and distal sodium reabsorption. At the same time, there was no relationship between the severity of proteinuria and the consumption of dietary protein, table salt, total and proximal sodium reabsorption, as well as urinary creatinine, urea, and electrolyte clearances. The results of the factor analysis revealed differences in the structure of the structure of mutual relationships between proteinuria, systolic blood pressure, creatinine, urea, and electrolyte clearance variables depending on the underlying disease. The magnitude of the partial correlation coefficients indicated that salt intake is accompanied by an increase in the excretion of all electrolytes, regardless of eGFR. CONCLUSION. Increased salt intake is formally accompanied by an increase in urinary excretion of all electrolytes. At the same time, sodium reabsorption increases, primarily proximal (hormone-independent). Hypernatremia does not develop, therefore sodium is deposited. One of the locations is the endothelium, which should cause a local inflammatory reaction that can support microcirculation disorders in the glomeruli with a gradual decrease in the excretory function of the kidneys. Probably, in addition to the classical indicators of CKD, it is worth adding a periodic calculation of dietary protein intake based on daily excretion of urea and table salt based on daily excretion of sodium and chloride.

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