The triad of protein leaking into the urine (proteinuria or albuminuria), rising blood pressure with hypertension and then falling renal function is common to many forms of CKD.

Protein loss in the urine due to damage of the glomeruli may become massive, and cause a low serum albumin with resulting generalized body swelling (edema) so called nephrotic syndrome.

Likewise, the estimated glomerular filtration rate (eGFR) may progressively fall from a normal of over 90 ml/min/1.73m2 to less than 15, at which point the patient is said to have end-stage renal disease.

[7] Pathophysiologic abnormalities in diabetic nephropathy usually begin with long-standing poorly controlled blood glucose levels.

[8] Initially, there is constriction of the efferent arterioles and dilation of afferent arterioles, with resulting glomerular capillary hypertension and hyperfiltration particularly as nephrons become obsolescent and the adaption of hyperfiltration paradoxically causes further shear stress related damage to the delicate glomerular capillaries, further proteinuria, rising blood pressure and a vicious circle of additional nephron damage and decline in overall renal function.

[11] The status of diabetic nephropathy may be monitored by measuring two values: the amount of protein in the urine - proteinuria; and a blood test called the serum creatinine.

The value of the serum creatinine can be used to calculate the estimated glomerular filtration rate (eGFR), which reflects the percentage of glomeruli which are no longer filtering the blood.

Other symptoms include tiredness, headaches, a general feeling of illness, nausea, vomiting, frequent daytime urination, lack of appetite, itchy skin, and leg swelling.

[2] The clinical presentation of diabetic nephropathy (DN) is characterized by proteinuria (protein in the urine), hypertension and progressive loss of kidney function.

This fibrosis is a product of multiple mechanisms including renal hemodynamic changes, glucose metabolism abnormalities associated with oxidative stress as well as inflammatory processes and an overactive renin-angiotensin-aldosterone system (RAAS).

This leads to a decrease in the delivery of sodium chloride to the macula densa in the distal tubules, promoting the release of renin and over-activating RAAS.

[citation needed] Diagnosis is based on the measurement of abnormal levels of urinary albumin in an individual with diabetes [27] coupled with exclusion of other causes of albuminuria.

To clinically stage the degree of damage in this (and any) kidney disease, the serum creatinine is determined and used to calculate the estimated glomerular filtration rate (eGFR).

The main components of managing cardiovascular disease is with tobacco cessation, lipid-lowering therapies (e.g., statins) as well as regular exercise and healthy eating.

Angiotensin-converting-enzyme inhibitors, as well as angiotensin II receptor blockers, are particularly helpful in patients with diabetes to lower blood pressure and slow the progression of nephropathy.

[42] Some patients might require dual therapy to adequately control pressure, in which case calcium channel blockers or diuretics are a good second-line option.

[44] Although RAAS blockade using more than one agent may further reduce proteinuria, the risk of adverse events (such as hyperkalemia, acute kidney injury) outweigh the potential benefits.

This means that as kidney function worsens in the setting of DN, some patients with insulin-dependent DM may find that their regular insulin doses are lasting longer than normal, or that they are experiencing an increasing frequency of hypoglycemic episodes.

[48] Patients with diabetic nephropathy might go on to develop end stage renal disease and require kidney transplantation or hemodialysis.

[51] The success of diabetic nephropathy management depends greatly upon the ability of individuals to self-manage this condition, encompassing glycaemic control, and the adoption of healthy lifestyles.

However, there is still insufficient evidence to draw conclusions regarding the effects, regarding both benefits and harms, of educational programmes for people with diabetic nephropathy.

[55] Diabetic kidney disease progression could lead to ESRD as well as an increased risk of cardiovascular complications, all of which cause a substantial economic burden.