The kidney in T2DM is not a "tenth-year complication". Some people arrive at diagnosis already with albuminuria. The morphological anchor that the course must name is diabetic glomerulosclerosis: thickening of the glomerular basement membranes, mesangial expansion, in the advanced form nodular Kimmelstiel–Wilson sclerosis, plus tubulointerstitial fibrosis and tubular atrophy. The clinician almost never starts with a biopsy. They start with two numbers that KDIGO and ADA both require: eGFR and UACR.
UACR is the ratio of albumin to creatinine in a random urine sample, in mg/g or mg/mmol. The KDIGO categories, also used by ADA:
| Category | UACR | Meaning |
|---|---|---|
| A1 | <30 mg/g (<3 mg/mmol) | normal / mildly increased |
| A2 | 30–300 mg/g (3–30 mg/mmol) | moderately increased |
| A3 | >300 mg/g (>30 mg/mmol) | severely increased |
The word "microalbuminuria", still used in the MoH RK 2022 protocol, has been replaced in KDIGO by A2: the same range, a different label. Do not mistake A2 for "unimportant". Even moderate albuminuria moves a person on the KDIGO heat map into a zone of higher risk of CKD progression and cardiovascular events — this is risk stratification, not proof that "30 mg/g will lead to dialysis tomorrow".
eGFR is the estimated glomerular filtration rate, mL/min/1.73 m². Categories G1–G5: G1 ≥90, G2 60–89, G3a 45–59, G3b 30–44, G4 15–29, G5 <15. CKD is diagnosed with a persistent reduction of eGFR <60 and/or persistent albuminuria (A2 or A3), as a rule confirmed, plus other markers of kidney damage. The ADA/KDIGO 2022 consensus emphasises: a persistent abnormality of UACR or eGFR (or both) is CKD and should lead to the immediate start of evidence-based treatment, not to "let's observe for a year".
Screening. ADA 2026, 11.1a: UACR and eGFR annually in everyone with T2DM, regardless of treatment. MoH RK 2022 protocol: the same frequency (once a year), worded as "albumin-to-creatinine ratio". One cannot replace the other: a normal creatinine does not exclude A3, and a normal UACR does not exclude G3.
Why renin–angiotensin system (RAS) inhibitors appear here before the "nephrologist". ADA 2026 Recommendation 10.8: an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB) is first-line treatment of hypertension in diabetes with albuminuria or coronary artery disease. Recommendation 10.10 (2026 revision): an ACE inhibitor or ARB is strongly recommended with severely increased albuminuria and/or eGFR <60 — at the maximum tolerated dose, to slow progression of kidney disease and reduce cardiovascular events. KDIGO 2022 keeps RAS blockade as the foundation of a comprehensive strategy together with an SGLT2 inhibitor.
The link to therapy that cannot be postponed until Module 4. CREDENCE (Perkovic et al. N Engl J Med. 2019; PMID 30990260): 4401 people with T2DM, eGFR 30–<90, UACR >300–5000 mg/g, all on RAS blockade; canagliflozin 100 mg vs placebo; median 2.62 years; primary composite endpoint (kidney replacement therapy (KRT) / eGFR <15 / doubling of creatinine / renal or cardiovascular death) — hazard ratio (HR) 0.70 (0.59–0.82). The population was albuminuric CKD, not "any T2DM with eGFR 88 and UACR 15". FLOW (Perkovic et al. N Engl J Med. 2024; PMID 38785209): 3533 people with T2DM and CKD (eGFR 50–75 with UACR 300–5000, or eGFR 25–<50 with UACR 100–5000); semaglutide 1 mg weekly; median 3.4 years; primary composite kidney-cardiovascular endpoint — HR 0.76 (0.66–0.88). The FLOW population is not "everyone with diabetes" but people at high renal risk.
Biopsy remains for the atypical: rapid decline in eGFR, active urinary sediment, systemic signs of another glomerulonephritis, absence of retinopathy with "severe nephropathy" — when the clinical picture does not fit diabetic glomerulosclerosis. Routine biopsy "to see the nodules" does not appear in the course's protocols.
The conclusion. Glomerulosclerosis is the morphological name of what the clinician catches with the pair UACR + eGFR. A missed UACR is a missed risk category and a missed start of nephroprotection.