What is Subacute Diffuse Glomerulosephritis?
Subacute diffuse glomerulosephritis has a malignant course and, as a rule, ends in the death of patients after 0.5-2 years from the onset of the disease. Apparently, the activity of immunological reactions is crucial for the occurrence of a malignant course of subacute glomerulonephritis.
Symptoms of Subacute Diffuse Glomerulosephritis
The disease usually begins as acute glomerulonephritis (often violently), but may occur latently at first. Characterized by large persistent edema, severe albuminuria (up to 10-30 g / l), as well as pronounced hypoproteinemia (45-35 g / l) and hypercholesterolemia (up to 6-10 g / l), i.e., signs of lipoid-nephrotic syndrome. At the same time, pronounced hematuria with oliguria is observed. With the latter, the relative density of urine is high only at the beginning, and then it becomes low. Renal filtration function progressively decreases. From the first weeks of the disease, azotemia can increase, which leads to the development of uremia.
Arterial hypertension with this form of nephritis is very high and is accompanied by severe changes in the fundus (retinal hemorrhage, optic nerve disc edema, the formation of exudative white retinal spots).
From the first weeks of the disease, azotemia can increase, which leads to the development of uremia. Arterial hypertension with this form of nephritis is very high and is accompanied by severe changes in the fundus (retinal hemorrhage, optic nerve disc edema, the formation of exudative white retinal spots).
Diagnosis of Subacute Diffuse Glomerulosephritis
The diagnosis is made, given the rapid development of renal failure, persistent severe arterial hypertension, often current in malignant type. Due to the fact that the syndrome of malignant hypertension can be observed with hypertension and with a number of kidney diseases – occlusive lesions of the renal arteries (especially often), chronic pyelonephritis, as well as in extrarenal diseases (for example, with pheochromocytoma), subacute gpomeruponephritis has to be differentiated with them. Subacute glomerulonephritis is indicated by the high severity of edematous-inflammatory and lipoid-nephrotic syndromes.
Treatment of Subacute Diffuse Glomerulosephritis
Treatment with steroid hormones of this form of glomerulonephritis is less effective, and in some cases is not indicated due to high and progressive arterial hypertension (blood pressure above 200/140 mm Hg). Recently, it is recommended to use antimetabolites and immunosuppressants (6-mercaptopurine, azathioprine, as well as cyclophosphamide) with careful monitoring of the morphological composition of the blood. Treatment with immunosuppressants is more effective in combination with corticosteroid hormones, which are prescribed in lower doses (25-30 mg / day). This combination not only contributes to the effectiveness of treatment, but also reduces the risk of complications from both corticosteroids and immunosuppressants (in particular, severe leukopenia).
To combat edema and arterial hypertension, hypothiazide is used (50-100 mg / day). The purpose of other antihypertensive drugs is also shown: dopegitis, reserpine, clonidine. In this case, a sharp decrease in blood pressure should be avoided, as this can lead to a deterioration in the filtration function of the kidneys. With an increase in renal failure and an increased content of nitrogenous slags in the blood, it is necessary to reduce the intake of protein with food and introduce large amounts of concentrated glucose (80-100 ml of a 20% w / w solution), as well as a 5% glucose solution of 300-500 ml w / v drip. In the absence of edema, 100-200 ml of 5% sodium bicarbonate solution should be dripped. In case of signs of heart failure, digitalis preparations and diuretics are prescribed. The use of dialysis (peritoneal or artificial kidney) is less effective than with chronic glomerulonephritis, due to the high activity and speed of progression of the main renal process. A kidney transplant is not indicated.
The prognosis of subacute glomerulonephritis is poor. This disease, as a rule, ends fatally after 6 months, but no later than 2 years later. Death occurs from chronic renal failure and uremia, less commonly from cerebral hemorrhage.