Diabetic nephropathy (zoafe kulya bawajah ziabetes shakari) is kidney disease or damage that results as a complication of diabetes. The exact cause of diabetic nephropathy is unknown, but it is believed that uncontrolled high blood sugar leads to the development of kidney damage, especially when high blood pressure is also present. In some cases, genes or family history may also play a role. Not all persons with diabetes develop this condition.
Each kidney is made of hundreds of thousands of filtering units called nephrons. Each nephron has a cluster of tiny blood vessels called a glomerulus. Together these structures help remove waste from the body. Too much blood sugar can damage these structures, causing them to thicken and become scarred. Slowly, over time, more and more blood vessels are destroyed. The kidney structures begin to leak and protein (albumin) begins to pass into the urine. Clinically, DN is characterized by a progressive increase in proteinuria and decline in GFR, hypertension, and a high risk of cardiovascular morbidity and mortality.
The earliest clinical evidence of nephropathy is the appearance of low but abnormal levels (>30 mg/day) of albumin in the urine, referred to as microalbuminuria, and patients with microalbuminuria are referred to as having incipient nephropathy. Diabetic nephropathy is a leading cause of end stage renal failure. The pathogenesis of diabetic nephropathy is multifactorial with contribution from metabolic abnormalities, homodynamic alteration, and various growth factors and genetic factors. Epidemiologic and family studies have demonstrated that family clustering and ethnicity plays an important role in the risk of developing this kidney disease.
It is estimated that up to 50% patients with diabetes mellitus will develop renal failure2. It is now firmly established that diabetic nephropathy is associated with high morbidity and mortality3. There is marked heterogeneity in the clinical picture seen in long termed diabetes as some diabetic patients even with poor metabolic control may not develop clinical diabetic nephropathy4.
Ancient Unani physicians estimated kidneys as pivotal organ and zoafe kulya is a secondary disease to absorb and filter the urine from blood i.e. blood purification. The current study is taken for the first time and considers the assessment of the scientific validity of the Unani medicines by applying modern parameters.
RISK FACTORS FOR DEVELOPMENT AND PROGRESSION OF DIABETIC NEPHROPATHY
Before the widespread aggressive treatment of blood pressure and hyperglycaemia, between 25% and 40% of both type 1 and type2 patients developed diabetic nephropathy over the course of25 years5,6,7 and risk factors that differentiate this subgroupfrom patients who maintain normal renal function are systemichypertension, glycaemic control, gender (M>F), genetic factors, hyperlipidaemia, dietary protein intake and smoking.
Hypertension is much more common amongst diabetic patients thanin the general population and has been identified as a major risk factor for both macrovascular and microvascular complicationsincluding diabetic nephropathy. Total cardiovascular mortalityin diabetes is strongly associated with raised blood pressure, particularly in type 2 disease.
Hypertension is strongly associated with insulin resistance, even in the absence of diabetes, and some 40-70% of type 2 patients will become hypertensive during their disease8. Only 25% ofpatients with type 1 diabetes are hypertensive and many of these will already have microalbuminuria or overt nephropathy9. Nevertheless,in both type 1 and type 2 diabetes with overt nephropathy the rate of decline of renal function correlates strongly with hypertension10,11 andin microalbuminuric patients hypertension correlates with thedegree of albuminuria12. In both these situations antihypertensive therapy is beneficial. Furthermore in normoalbuminuric type1 diabetes small increases in blood pressure have been correlatedwith the subsequent development of microalbuminuria13. Therecan therefore now be little doubt that a raised blood pressureis a risk factor for the development and progression of diabetic nephropathy as well as a potent risk factor for cardiovascular morbidity and mortality.
Type 1 and type 2 diabetes have in common the state of chronic hyperglycaemia,and glucose- dependent processes are likely to be involved in the pathogenesis of diabetic complications, including nephropathy. Glucose- inducedtissue injury may be mediated by the generation of advanced glycated proteins or via other mechanisms such as the polyol pathway,both of which have been implicated in nephropathy14. Consistentwith this hypothesis are observational studies correlating haemoglobinA1c (HbA1c) concentration with the development and progressionof microalbuminuria and overt nephropathy13.
Proteinuria is generally regarded as a marker for the degree of glomerular damage: the level of proteinuria correlates wellwith the prognosis for renal function, and interventions that retard the progression of diabetic renal disease also reduceproteinuria. However, we do not yet know whether the flux ofprotein across the glomerular basement membrane is causally implicated in the evolution of diabetic renal disease or simplyreflects glomerular damage15.
Genetic factors are likely to be important in diabetic nephropathy.Recent interest has focused on genes of the renin angiotensinsystem, which are known to be highly polymorphic and have been extensively studied in relation to cardiovascular disease. Aninsertion(1)/ deletion(D) polymorphism in the ACE gene has been identified that is strongly associated with raised circulating ACE levels and with increased risk of coronary heart disease in non-diabetic individuals. Some studies have found the DD genotypeto be associated with an increased risk of diabetic nephropathy and a rapid decline of GFR in both type 1 and type 2 diabetes16.The clinical implications have yet to be explored. Other genetic loci that may be involved include the sodium—lithium exchanger and the sodium—hydrogen antiporter genes.
Hyperlipidaemia is common in both type 1 and type 2 diabetes.Raised plasma triglycerides and low levels of highdensity liproproteins(HDL) have been correlated with the development of diabeticnephropathy as well as with cardiovascular diabetic complications5,17,18. Triglycerideand cholesterol reduction, although important in reducing cardiovascular risk, has not been found to alter the progression of renal disease and the importance of hyperlipidaemia remains to be established in this respect.
The diabetic nephropathy management is done with medicines due to which kidneys are protected and the blood pressure is lowered. The kidney damage may be reversed and certain amount of urine can be found in the urine. If these medicines are used before the occurrence of nephropathy, it can be prevented in people who are having a normal blood pressure. The focus of the diabetic nephropathy treatment is on managing the high blood pressure and slowing down the progression of hypertension. The protein in the urine is also reduced. A customized treatment plan will also be received. These treatments will include:
- Management of proteinura;-The level of albumin can be reduced by medications. Albumin is a kind of protein. The kidney function can be improved.
- Management of high blood pressure:-The high blood pressure can be controlled by physical activity, diet and medications
- Controlling the blood sugar:-The blood sugar levels can be greatly controlled by physical activity, diet and medications. This is an effective diabetic nephropathy treatment.
- 4Medication review:-The current medications will be reviewed by the nurse specialists and nephrologists. The dosages may be adjusted and medications will be changed if necessary.
- Preventive measures for complications from the contrast dye studies :-Information will be received about the risk of increased kidney damage. These also include medical tests that will involve the use of contrast dye.
- Special plans for diet:-Nutrition advice and personalized dietary plan will be provided by the dietician. This will also include ways for including alcohol, caffeine, protein and salt.
- Treatment of anemia :-A person will be assessed for anemia. This also leads to the decrease in the number of red blood cells. The necessary medication is received.
- Bone health :-Medications and diet will help in managing the balance of calcium phosphate. This is very essential to maintain healthy bones.
- Anti- platelet therapy :-A low dose of daily aspirin may be prescribed by the doctor for preventing blood clots. This should be taken by a person till he doesn’t notice the side effects of aspirin.
- . Other lifestyle changes :- Information can also be provided about maintaining a healthy lifestyle. There are many programs such as weight management suggestions, exercise programs and programs for stopping smoking.