Conditions · Nephrology and urology
Diabetic kidney disease !
Kidney damage caused by years of diabetes. It is silent at first, shows up as albumin in the urine, and is a leading cause of dialysis.
Updated 2026-11-01
Structures involved
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In embryology
In the clinical exam
Why it happens
- Fibrosis in organs: TGF-β and the myofibroblast
- Intracellular accumulations: cholesterol, proteins, hyaline, glycogen
- Glomerular filtration: the barrier and its determinants
- Renal blood flow, autoregulation and tubuloglomerular feedback
- The renin–angiotensin–aldosterone system
- Glomerulus and the filtration barrier: podocytes, mesangium, JGA
What it is
Chronic kidney disease caused by diabetes, recognised by persistent albuminuria, a falling glomerular filtration rate, or both, in a person with long-standing diabetes and no other more likely cause. It is also called diabetic nephropathy.
Who gets it
Diabetes is one of the leading causes of chronic kidney disease and of dialysis worldwide. Colombia's Cuenta de Alto Costo keeps a national registry of chronic kidney disease, hypertension and diabetes and notes that kidney disease is more frequent in people with diabetes or hypertension. It affects a large share of people with type 2 diabetes and is often found late because it causes no symptoms.
Causes
- Chronic hyperglycaemia in type 1 or type 2 diabetes
- Glomerular hyperfiltration and intraglomerular hypertension
- Coexisting systemic hypertension that accelerates the damage
- Genetic susceptibility
Risk factors
- Long duration of diabetes and poor glycaemic control
- High blood pressure
- Smoking, obesity and high-salt diet
- Family history of diabetic kidney disease or kidney failure
- Indigenous, Hispanic and African ancestry in several cohorts
- Presence of diabetic retinopathy (shared microvascular damage)
Pathophysiology
High glucose and advanced glycation end products, with activation of the renin–angiotensin–aldosterone system, dilate the afferent arteriole and raise pressure inside the glomerulus (hyperfiltration). Over years the glomerular basement membrane thickens, the mesangium expands and nodular sclerosis (Kimmelstiel–Wilson nodules) forms, with hyaline arteriolosclerosis of afferent and efferent arterioles. Albumin leaks into the urine and nephrons are progressively lost, so the GFR falls.
Classification
- By KDIGO GFR category (G1–G5) and albuminuria category: A1 normal (under 30 mg/g), A2 moderately increased (30–300 mg/g, formerly microalbuminuria), A3 severely increased (over 300 mg/g)
- Classic stages: hyperfiltration, silent phase, moderately increased albuminuria, overt proteinuria, kidney failure
Symptoms and signs
- No symptoms in early stages; detected by screening
- Foamy urine when proteinuria is heavy
- Oedema of legs and face
- Worsening blood pressure control
- In advanced disease: fatigue, nausea, itching, loss of appetite, shortness of breath
- Fewer insulin needs or more hypoglycaemia as kidney function falls
Diagnosis
- Clinical
- Long-standing diabetes, often with retinopathy, plus persistent albuminuria or a reduced eGFR on at least two occasions over 3 months; blood pressure and volume status.
- Tests
- Yearly screening with urine albumin-to-creatinine ratio (spot sample) and serum creatinine with eGFR, in type 2 diabetes from diagnosis and in type 1 from about 5 years after onset; potassium, HbA1c, lipids, haemoglobin, and calcium, phosphate and parathyroid hormone in advanced stages. Biopsy only when another cause is suspected.
- Imaging
- Kidney ultrasound (kidneys are often normal or enlarged in size, unlike most other CKD causes) and fundus examination for associated retinopathy.
Differential diagnosis
- Hypertensive nephrosclerosis
- Other glomerular diseases in a person with diabetes (membranous nephropathy, IgA nephropathy)
- Renovascular disease (renal artery stenosis)
- Obstructive uropathy or chronic pyelonephritis
- Drug-induced nephropathy (NSAIDs)
Goal of treatment
Slow the loss of kidney function and reduce cardiovascular risk by controlling glucose and blood pressure, lowering albuminuria and blocking the pathways that damage the kidney.
Treatment
- Medical
- ACE inhibitors or ARBs (not combined) for people with albuminuria and hypertension; SGLT2 inhibitors for kidney and heart protection when eGFR allows.
- Medical
- Added protection in selected people: a non-steroidal mineralocorticoid receptor antagonist (finerenone) or a GLP-1 receptor agonist; statins for cardiovascular risk.
- Medical
- Glucose-lowering drugs adjusted to eGFR (metformin limited at low eGFR, insulin needs may fall).
- Lifestyle
- Low-salt diet, protein intake that is adequate but not high, no smoking, physical activity, weight control; avoiding NSAIDs and limiting contrast exposure.
- Follow-up
- Regular eGFR, albuminuria and potassium, especially after starting or changing renin–angiotensin blockers; referral to nephrology as eGFR falls.
- Procedure
- Dialysis or kidney transplantation (sometimes with pancreas) in kidney failure.
Complications
- Progression to kidney failure needing dialysis or transplantation
- Cardiovascular disease, the main cause of death in these patients
- Hyperkalaemia and metabolic acidosis
- Anaemia of chronic kidney disease and mineral bone disease
- Nephrotic syndrome with heavy proteinuria
- Hypoglycaemia from reduced insulin clearance
Prognosis
With early detection, renin–angiotensin blockade, SGLT2 inhibitors and control of glucose and blood pressure, progression can be slowed a great deal and many people never reach kidney failure. Higher albuminuria and lower eGFR mean a higher risk of both kidney failure and cardiovascular death.
Prevention
- Good glycaemic and blood pressure control from the diagnosis of diabetes
- Yearly screening for albuminuria and eGFR in every person with diabetes
- Not smoking and avoiding nephrotoxic drugs
Test yourself
Think of the answer, then tap the question to see it.
What is the earliest laboratory sign of diabetic kidney disease?
Moderately increased albuminuria (urine albumin-to-creatinine ratio 30–300 mg/g), often with normal or high GFR.
Which glomerular lesion is characteristic of diabetic nephropathy on biopsy?
Nodular glomerulosclerosis (Kimmelstiel–Wilson nodules), with basement membrane thickening and hyaline arteriolosclerosis.
Which two drug classes are central to slowing diabetic kidney disease?
Renin–angiotensin blockers (ACE inhibitors or ARBs) and SGLT2 inhibitors.
Which electrolyte must be monitored after starting an ACE inhibitor or ARB?
Potassium (along with creatinine), because these drugs can cause hyperkalaemia.
When should screening start in type 1 versus type 2 diabetes?
About 5 years after diagnosis in type 1, and at diagnosis in type 2, then yearly.
Related conditions
- Type 2 diabetes mellitus
- Type 1 diabetes mellitus
- Chronic kidney disease
- Arterial hypertension
- Diabetic retinopathy
- Nephrotic syndrome
- Heart failure
- Acute kidney injury
- Hyperkalaemia
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Diabetic Kidney Disease - NIDDK (NIDDK (National Institutes of Health), 2024); Diabetes and kidney disease: MedlinePlus Medical Encyclopedia (MedlinePlus (U.S. National Library of Medicine), 2024); ERC - Cuenta de Alto Costo (Cuenta de Alto Costo (Colombia), 2026).
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