Diabetic kidney disease (DKD) is usually a clinical diagnosis in a patient with long-standing diabetes (>10 years) with albuminuria and/or reduced estimated glomerular filtration rate (eGFR) in the absence of signs or symptoms of other primary causes of kidney damage.
Symptoms, which may be absent until the disease is advanced, include fatigue, anorexia, and swelling of the extremities. Signs include hypertension, oedema, and findings of associated microvascular complications (diabetic retinopathy and neuropathy). In clinical uraemia, anorexia, encephalopathy, nausea and vomiting, dysgeusia (altered taste), bleeding, myoclonus and pericarditis are present.
Proteinuria is the characteristic laboratory finding. Deterioration in renal function may develop as the disease advances. However, the pattern of albuminuria and reduced glomerular filtration rate (GFR) is changing, and reduced GFR without albuminuria is becoming more common. Such patients usually have a better renal prognosis than those with overt albuminuria. In addition, progression of DKD may occur even in patients in whom control of diabetes mellitus has been achieved in accordance with diabetes guidelines.
Treatment includes intensive control of hyperglycaemia and hypertension with ACE inhibitors, angiotensin-II receptor antagonists, or other antihypertensives. Lipid reduction and smoking cessation may be beneficial. Sodium-glucose co-transporter 2 (SGLT2) inhibitors are mildly effective at glycaemic control, but are very effective at reducing proteinuria and slowing the progression of DKD.
Complications include hypoglycaemia due to intensive treatment of hyperglycaemia, hyperkalaemia as an adverse effect of ACE inhibitors or angiotensin-II receptor antagonists, volume depletion due to osmotic diuresis from glycosuria, and inadequate protein/caloric intake leading to malnutrition. Some patients may reach end-stage renal failure, requiring dialysis.
Diabetic kidney disease (DKD) is defined by albuminuria (increased urinary albumin excretion is defined as ≥3.4 mg/mmol [30 mg/g]) and progressive reduction in estimated glomerular filtration rate (eGFR) in the setting of a long duration of diabetes (>10 years' duration of type 1 diabetes; may be present at diagnosis in type 2 diabetes), and is typically associated with retinopathy. In most patients with diabetes, chronic kidney disease (CKD) can be attributable to diabetes if these features are met; however, CKD may be present without retinopathy in type 2 diabetes, and without albuminuria in type 1 and type 2 diabetes. Other cause(s) of CKD should be considered in the presence of rapidly increasing albuminuria or nephrotic syndrome, rapidly decreasing eGFR, active urinary sediment (e.g., cellular casts in urine), the absence of diabetic retinopathy in patients with type 1 diabetes, or signs or symptoms of other systemic disease. The diagnosis is most conclusively made by findings of mesangial expansion and nodular glomerulosclerosis on kidney biopsy, though it is rarely necessary.
History and exam
Key diagnostic factors
- presence of risk factors
- signs of retinopathy
Other diagnostic factors
- poor vision
- numbness of the lower extremities
- pain of the lower extremities
- constitutional symptoms (advanced disease)
- foot changes
- orthostatic hypotension
- skin changes
- muscular atrophy
- pallor (as glomerular filtration rate declines)
- bleeding tendency (advanced disease)
- Kussmaul's respirations (advanced disease)
- sustained hyperglycaemia
- family history of hypertension and/or kidney disease
- physical inactivity
- high protein, fat, and sodium intake
1st investigations to order
- urinary albumin to creatinine ratio (ACR)
- serum creatinine with GFR estimation
- kidney ultrasound
Investigations to consider
- albumin excretion rate (AER)
- CT abdomen
- magnetic resonance angiography (MRA)
- Doppler ultrasound
- kidney biopsy
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