scholarly journals Diabetic nephropathy: Pathogenesis and treatment

1996 ◽  
Vol 42 (4) ◽  
pp. 37-42
Author(s):  
A. V. Vorontsov ◽  
M. V. Shestakova

Currently, diabetic nephropathy (DN) is the leading cause of disability and mortality in patients with diabetes mellitus (DM). Developing in 4045% of patients, both insulin-dependent IDDM (type I) and non-insulin-dependent IDDM (type II) diabetes, this formidable complication leads to the development of chronic renal failure, and ultimately to the death of patients from uremia. The first kidney damage in diabetes was described by R. Kimmelstiel and C. Wilson in 1936. It is clinically characterized by the following manifestations: increasing proteinuria (with unchanged urinary sediment), hypertension, the formation of nephrotic syndrome (in about 30% of patients) and a progressive decrease in filtration kidney function. The insidiousness of this complication of diabetes lies in the fact that it develops gradually and remains unnoticed for a long time, since at the initial stages the patient does not cause discomfort. And in the later stages, when the presence of DN is no longer in doubt, preventing its further progression is extremely difficult, and often impossible. For many years in our country, the classification of DNs was used by V. R. Klyachko, according to which prenephrotic, nephrotic, and nephrosclerotic stages were distinguished. According to this classification, DN is diagnosed only from the moment when the patient develops proteinuria, registered by conventional laboratory methods, which indicates the severity and irreversibility of pathological changes in the kidneys. The modern classification, distinguishing stages at which clinical manifestations are still absent, and only functional disorders are detected, was proposed by S. Mogensen in 1983 (see table). In accordance with this classification, the first 3 stages are not detected by conventional clinical methods (preclinical stage of DN). The most informative marker of the early stages of DN is the determination of microalbuminuria (MAU), which means the excretion of albumin with urine in an amount of 30 to 300 mg / day. Identification of UIA in a patient with type I diabetes means that the probability of developing a clinical picture of DN in his next 10 years is 80%.

1996 ◽  
Vol 42 (3) ◽  
pp. 3-6
Author(s):  
M. I. Balabolkin ◽  
G. G. Mamayeva ◽  
V. Yu. Evgrafov ◽  
L. I. Lyudina ◽  
N. A. Bishele

A total of 107 diabetics were examined using general clinical methods, assessment of microalbuminemia, Rehbergs test for renal function, coagulogram, thromboelastogram, lipid spectrum of the serum, and ophthalmological examination. The stages of diabetic nephropathy and retinopathy and degree of the major pathological changes in the retina were found to be in direct correlation. Initial diabetic retinopathy was found to develop earlier than nephropathy in the majority of patients, and preproliferative and proliferative retinopathy was appreciably more incident in the presence of diabetic nephropathy. Changes in the fundus oculi were more expressed in patients with type I diabetes and nephropathy than in those with type II condition. At the same time, the development of diabetic nephropathy was associated with deterioration of the fundus oculi parameters only in diabetics with type II condition, whereas in those with type I disease it influenced only the number of microaneurysms. The progress of diabetic nephropathy with increase of proteinuria may be caused by such risk factors as microcirculatory disorders and changes in the lipid spectrum of the blood serum.


2001 ◽  
Vol 47 (3) ◽  
pp. 15-18
Author(s):  
O. Ye. Voronko ◽  
D. A. Chistyakov ◽  
К. V. Savostyanov ◽  
L. A. Chugunova ◽  
M. Sh. Shamkhalova ◽  
...  

Distribution of alleles and genotypes of microsatellite D6S392 neighboring mitochondrial superoxide dismutase (SOD2) gene and of two polymorphous markers (minisatellite ecNOS4a/4b and mutation in codone 298: replacement of glutamic acid (Glu) with asparaginic (Asp) acid) was studied in patients with insulin dependent diabetes mellitus (IDDM) with and without diabetic nephropathy (DN) (36 and 56 patients, respectively). Distribution of locus D6S392 alleles and polymorphous marker Glu298Asp was virtually the same in both groups. Differences were observed for minisatellite ecNOS4a/4b. In DN patients the content of allele 4a and of genotype 4a/4b is increased in comparison with patients without DN (38.9 vs. 22.3%, p < 0.02, and 61.1 vs. 41.7%, p < 0.05, respectively). Decrease in the percent age of 4b/4b genotype and allele 4b in DN patients are also significant (30.6 vs. 57.1%, p < 0.02, and 61.1 vs. 77.1%, p < 0.02). Hence, polymorphous site ecNOS4b/4a of NOS3 gene is associated with DN development in patients with IDDM living in Moscow.


1991 ◽  
Vol 37 (12) ◽  
pp. 2027-2028 ◽  
Author(s):  
Nelson B Watts

Abstract The lifetime risk of diabetic nephropathy is ˜45% for patients with Type I (insulin-dependent) diabetes (1) and at least 30-35% for patients with Type II (non-insulin-dependent) diabetes (2, 3). In Type I diabetes, the incidence of readily detectable nephropathy rises steeply 10 years after the onset of diabetes (1). The progression from the appearance of “clinical proteinuria” (a positive test for protein upon routine urinalysis) to end-stage renal failure requiring dialysis or kidney transplantation occurs over about five years. This progression is usually relentless (4), but the rate of deterioration may be slowed or stabilized with improved glucose control (5-7), by the use of angiotensin-converting enzyme inhibitors (8, 9), diltiazem (10) [but not nifedipine (11)], and dietary protein restriction (12). Early intervention, before the development of clinical proteinuria, appears to be much more effective than later treatment.


1988 ◽  
Vol 25 (2) ◽  
pp. 161-172 ◽  
Author(s):  
Roberto Torella ◽  
Teresa Salvatore ◽  
Domenico Cozzolino ◽  
Franco Grandillo ◽  
Dario Giugliano

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