[Risk factors and pathogenetic mechanisms of left ventricular hypertrophy in progressive chronic kidney disease and after transplantation of the kidney].

AIM: To specify the trend in the incidence of left ventricular hypertrophy (LVH) at a predialysis stage of chronic kidney disease (CKD) in the course of its progression from stage III to stage V and after transplantation of the kidney (TK); to study correlations between homeostatic disorders caused by CKD progression and myocardial remodeling; to define the role of some hemodynamic and nonhemodynamic factors in formation of LVH. MATERIAL AND METHODS: The study enrolled 128 patients (58 males and 70 females, age 18-55 years, mean age 42 +/- 11 years) at a predialysis stage of CKD (group 1) and 225 recipients of renal allotransplant--RRA (group 2, 140 males and 85 females, age 18-69 years, mean age 43 +/- 12 years). General clinical examination, biochemical and immunological blood tests, echocardiography were made. RESULTS: At a predialysis stage of CKD, LVH was diagnosed in 56% patients. Incidence of LVH was directly related with age of the patients (p = 0.001), blood pressure (p < 0.001), duration of arterial hypertension (p = 0.004), severity of anemia (p = 0.017), the level of C-reactive protein (p = 0.003), blood phosphorus concentration and inversely correlated with glomerular filtration rate--GFR (p = < 0.001), albumin level (p = 0.023) and blood Ca (p < 0.001). LVH was followed up for 12 months in 35 patients with predialysis CKD. Factors of LVH progression and factors hindering its regression were systolic blood pressure, Hb and Ca in the blood. In group 2 of RRA incidence of LVH was 53%. Significant factors of LVH risk after transplantation were age (p = 0.002), hypertension (p = 0.005) and anemia (p = 0.04). Moreover, LVH closely correlated with proteinuria (p < 0.03), transplant dysfunction (p = 0.002) and posttransplantation ischemic heart disease (p < 0.037). Changes in LVH were analysed in 30 RRA. Frequency of LVH decreased for 2 years after transplantation (from 56 to 32%) but 36-60 and more months after transplantation it increased (46 and 64%, respectively). Transplant dysfunction was the leading factor hindering LVH regression after transplantation. CONCLUSION: The same mechanisms are involved in LVH pathogenesis after transplantation and at a predialysis stage of CKD. The significance of initial renal lesion signs--minimal proteinuria and hypercreatininemia--was higher after renal transplantation than in patients with CKD.

[The structure of causes of acute renal failure and the efficacy of its treatment according to the materials of an intensive nephrological care unit].

The study was undertaken to study the frequency, causes, and efficiency of treatment for acute renal failure (ARF) at the intensive nephrological care unit. The data on 117 patients with ARF of various etiology were studied. In them, ARF was caused by acute interstitial nephritis in 18.8%, by urosepsis in 18.8%, by non-urological sepsis in 19%, by destructive pancreatitis in 18%, in 13% rapidly progressive glomerulonephritis was present in systemic vasculitis. In 8.5% of the patients, ARF developed as a complication of severe pneumonias along with respiratory failure. Only single cases were presented with ARF of other intoxication etiology, crush syndrome, or acute vascular diseases. Renal replacement therapy was used in all cases. Its mode (intermittent or low-flow continuous) was determined by the severity of renal failure and the general condition of patients. The overall mortality was 38% in the whole group. It was 55% in sepsis, 33% in destructive pancreatis, 8.3% in urosepsis, 8% in acute interstitial nephritis, 64.7% in rapidly progressive glomerulonephritis. According to the type of therapy, there were no significant differences in mortality rates. There was also a correlation of the mortality rates and the APACHE score.