[Clinical management of the patient affected with acute renal failure (ARF) secondary to volume depletion]. / Gestione clinica del paziente con insufficienza renale acuta (IRA)da ipovolemia.

Most cases of ARF are secondary to volume depletion. In the literature, very few scientific publications address the problem of what to do when confronted with such a patient. As regarding the diagnosis of hypovolemia, an accurate history and physical examination can help to determine both the presence and etiology of volume depletion; postural hypotension (decrement in systolic blood pressure of more than 20 mmHg after standing from the supine position), associated with a pulse increment of 30 beats/min or more and dizziness are specific symptoms of hypovolemia. Laboratory indices are useful to diagnose volume depletion, but their interpretation is not simple, and they may not be available in the non-nephrologic environment. Fluid replacement therapy in hypovolemia is largely dependent upon the type of fluid that has been lost and concurrent electrolytic and acid-base disorders. Patients with hypernatremia and volume depletion should receive mild hypotonic solutions, whereas those with hyponatremia and hypovolemia should receive mild hypertonic solutions. The entity of reinfusion depends on daily losses. Conversely, monitoring of body weight can be considered an adequate index of fluid balance. Concerning the treatment of ARF, the use of loop diuretics in the early phases of pre-renal ARF decrease oxygen consumption in the tubular cells by inhibiting transcellular sodium transport, therefore preventing or limiting ischemic cell injury. The use of loop diuretics should also be evaluated in intermediate syndrome and ischemic NTA where diuretics can, respectively, reduce renal ischemia and convert oliguric ARF into the non-oliguric form.

[Acute and chronic effects of standard hemodialysis and soft hemodiafiltration on interdialytic serum phosphate levels]. / Effetti acuti e cronici della emodialisi standard e dell'emodiafiltrazione-soft sui livelli interdialitici della fosforemia.

INTRODUCTION: The dialytic management of hyper-phosphoremia, which is inadequate because of insufficient intra-dialytic removal of phosphate (P), is further limited by PDR-P, i.e. the significant increase in serum P levels during the early postdialytic period. Patients and methods. To investigate the effects of enhanced P removal by haemodiafiltration on the inter-dialytic phosphoremia, we studied 12 uremic patients that were switched, with cross-over randomised modality, to a single session of standard hemodialysis (HD) and hemodiafiltration (HDF) (Acute Study). Blood samples were obtained before the treatment, at the end (T0), after 30, 60, 90 and 120 minutes, and at 24, 48 and 68 hours. During both dialytic treatments the whole effluent dialysate was collected to evaluate the intradialytic removal of P. Thereafter, patients were randomised to receive either HD or HDF for three months, in the presence of constantly similar Kt/V, food intake and dose of phosphate binder (Chronic Study). RESULTS: Acute Study. Compared to HD, P removal in HDF was about 44% greater in the presence of identical predialytic P levels (6.0+/-0.2 and 5.9+/-0.4 mg/dl) and Kt/V (1.35+/-0.06 and 1.34+/-0.05); however, the inter-dialytic decline of serum P levels did not differ (-50+/-3% versus -42+/-3%, p=0.098). In HDF, PDR-P was faster (30 min versus 90 min) and better (at T120: +69+/-6% versus +31+/-4%, p<0.001). The higher P levels were maintained throughout the inter-dialytic period whereas Ca x P changed in parallel. Chronic Study. During the three months, pre-dialytic serum P diminished in HDF (from 5.8+/-0.2 to 4.4+/-0.3 mg/dl, p<0.05), while it remained unchanged in HD. A similar pattern of changes was detected in Ca x P. CONCLUSIONS: Enhancement of P removal, acutely amplifies the extent of PDR-P, but allows better control of Ca-P homeostasis in the medium term. This effect is likely to be dependent on the enhanced mobilisation of phosphate from a deep compartment.

Diagnosis of renal disease at the beginning of the 20th century.

At the beginning of this century, the diagnosis of various renal diseases was made with relative accuracy although neither plasma markers of glomerular filtration nor renal biopsy nor imaging were available. Renal edema was identified by high albuminuria, hyalin cylinders, high urine density and oliguria. Renal hematuria was detected by cylinders of erythrocytes. Hallmarks of chronic renal insufficiency, recognized at autopsy by atrophic kidneys, were hyposthenuria, polyuria and slight albuminuria without edema associated with arterial hypertension, anemia, retinopathy and left ventricular hypertrophy. The detection of increased plasma volume in experimental toxic nephritis by St. Moscati proposed the underlying mechanism of arterial hypertension. Experimental and clinical research in the preinsulin era indicated the central role of the kidney in the functional alterations induced by diabetes. Indeed, glucosuria was known to appear only when glycemia was relatively high. The kidney appeared enlarged and hyperemic, i.e. the so-called glomerular hyperfiltration. Glucosuria was directly correlated with diuresis but it markedly decreased in renal insufficiency. In diabetes complicated by nephropathy, tolerance to carbohydrates improved. Correction of glucosuria by dietary treatment was followed by a prompt rise in body weight, due to retention that counterbalanced the previous losses. Diabetic ketoacidosis, determined by the measurement of urinary ketonic body excretion, was treated with sodium bicarbonate (30-50 g/day in severe acidosis) up to achieving an alkaline urine pH. It was known that high doses of sodium bicarbonate might induce edema which gradually disappeared with a reduction in the alkaline administration. Clinical significance of sodium balance was, in fact, recognized: the external NaCl balance between alimentary ingestion and urinary excretion was neutral in normal conditions and became positive at high body temperature or negative during reabsorption of exudates.