Managing CKD and diabetes risk in young patients: eGFR trajectory, blood pressure, and early aggressive care

Professor Merwin (as Otter named them) — diabetes / diabetic complications

Otter intro: clinician scientist and program leader in the Department of Diabetes at Monash University; fellow of the Australian Academy of Health and Medical Sciences (Otter: “Australian Academy of Medicine Science”); founder of Range Biotech; research focused on mechanisms of diabetic complications and prevention/treatment opportunities. Otter also wrote “Merlin” once in the welcome line — we keep Merwin as the primary byline and do not invent a surname.

Ralph Alder — GP co-host (fireside chat)

Otter intro also garbled a GP partner as “Ram Aldo” (35 years’ experience; honorary clinical associate professor, University of Melbourne Department of General Practice; chronic disease, diabetes, heart disease, transition research). Seminar framing treats Ralph Alder as the GP interlocutor in the fireside chat.

Host / chair

Healthed seminar introduction (Ralph Alder named in opening; “Dave” thanked briefly on stage).

Clinical case: 35-year-old with “OK” numbers

The fireside chat centres on a 35-year-old man with hypertension for two years (father’s hypertension began around age 40). Both parents have type 2 diabetes; father had an AMI. He is a non-smoker who vapes. He is on perindopril 5 mg, feels tired after work but not daytime-sleepy, and has occasional palpitations when rushing for the train — no chest pain.

Clinic snapshot presented in the talk:

• Clinic BP about 138 systolic — “not terrible,” but not ideal for 35
• BMI 34; general examination otherwise normal
• HbA1c 5.7% (was 5.5% two years earlier) — drifting the wrong way
• eGFR 65 now; 71 twelve months ago
• UACR about 3.8 then 3.5 a week later (mg/mmol in KDIGO framing)
• Lipids: LDL 2.8, HDL 0.9, triglycerides 2.1 (non-fasting)
• Abnormal LFTs consistent with fatty liver; FIB-4 “okay” (not advanced fibrosis)
• MSU normal (no blood, no white cells); ultrasound framed as normal in discussion
• Five-year absolute CV risk calculator ~3% — looks “low” until you remember he is 35

Why eGFR 65 is not fine at 35

Professor Merwin’s punchline: ask why a 35-year-old is even in the GP room with treated hypertension and a falling eGFR. Family history is “bugging” him — and the numbers justify that worry.

On a KDIGO-style heat map, eGFR 60–89 with modest albuminuria can sit in a green box. That colour is calibrated for population risk banding, not for age-expected kidney “reserve.” Analogy from the talk: osteoporosis uses a T-score (vs young adult peak) and a Z-score (vs age peers). An eGFR of ~60 is like a T-score of about −2 (“thin kidneys”). At 35, his age-matched expectation should be in the 90s — so his “Z-score” is also deeply abnormal. Dropping from 71 → 65 over a year is a second red flag.

Albuminuria: nothing is “mild” on a heat map

UACR ~3.5–3.8 sits just into the microalbuminuria / A2 range (threshold often taught as ~3 mg/mmol). The GP instinct is to say “a tad” or “mild.” The specialist push-back: KDIGO heat maps are about risk stacking, not mild/moderate/severe labels. Combined with young age, treated hypertension, falling eGFR, obesity, and family history, that “tad” is part of a louder signal.

Lipids, liver, and the CV calculator trap

Dyslipidaemia fits BMI 34: fat not stored safely ends up in circulation (higher triglycerides). Abnormal LFTs with a reassuring FIB-4 still point to MASLD (metabolic dysfunction–associated steatotic liver disease; formerly “fatty liver”) and possibly inflammatory MASH — without advanced fibrosis. The lecture’s key epidemiologic point: people with MASLD/MASH more often face heart, stroke, and kidney disease than liver failure. The fatty liver is a canary in the coal mine for shared cardiometabolic injury.

Absolute CV risk ~3% looks low because calculators are not calibrated for healthy 35-year-olds. Thirty-five-year-olds “should” be near zero five-year risk. With this family history and organ damage markers, 3% is not reassuring.

Trajectory beats a single green square

Natural history matters more than one heat-map colour. Losing about 7 mL/min/1.73 m² per year (71 → 65) on current therapy, if sustained, projects toward kidney failure in roughly a decade — still in middle age. Thresholds emphasised in the chat: decline faster than about 3 mL/min/year, or ~10 mL over three years (e.g. 70 → 60), is “way too fast” and needs slowing.

Practical barriers: many public nephrology pathways will not accept this man yet (eGFR not low enough / not “classic” referral criteria). That is framed as a tragedy — he may have kidney disease (possibly familial) that GPs will have to manage while tracking slope, not waiting for eGFR <30.

Blood pressure, nocturnal dipping, and SPRINT nuance

Clinic BP 138 may be falsely reassuring: medication taken before the visit, relaxed consulting room calm — while vaping spikes or nocturnal non-dipping may be much higher in real life. Prefer home or 24-hour ambulatory BP, including night-time behaviour. People with CKD often lose the normal nocturnal dip that supports cardiovascular and kidney stability.

ACE inhibitors remain foundational for albuminuric kidney disease, but some ACE inhibitors are relatively short-acting: daytime coverage without solid night coverage. Preference expressed in the talk: longer-acting ARBs when nocturnal control is the priority (still individualise). Hypertension here may be a symptom of CKD as much as a cause — ultrasound/MSU normality does not exclude intrinsic kidney disease; still consider familial polycystic disease in young hypertensives with falling GFR.

SPRINT nuance (non-diabetic cohort; subgroup with lower eGFR and limited albuminuria): aiming systolic into the intensive range improved mortality, but kidney outcomes (doubling of creatinine / decline) were not improved — if anything, creatinine rose more with aggressive lowering. ADVANCE/ACCORD lessons in diabetes: aggressive BP reduces stroke risk, but rate of kidney-function decline is not dramatically rescued by BP alone. Conclusion in the chat: treat BP well, but BP alone is not enough — treat the underlying CKD drivers.

Obesity vs the whole kidney story

Obesity accelerates kidney decline and can raise albuminuria, but classic obesity-related kidney injury often starts with hyperfiltration (high GFR) then scarring — not an already-low eGFR at 35. Clinical obesity (high BMI plus metabolic dysfunction) is present here, and weight loss should help BP, liver fat, dysglycaemia, and free fatty acid load on residual nephrons. The lecturer’s caution: weight loss is necessary but may not be sufficient to explain or fix this man’s trajectory — investigate and treat as CKD, not “just fat.”

Lost nephrons do not grow back. Albuminuria can improve; eGFR does not “return” — modern language is preserving residual function, not magically reversing decline. Reduce the overtime burden on remaining nephrons (BP spikes, lipids, glucose, free fats, obesity).

SGLT2, GLP-1, and Australian label realities

KDIGO-style pillars recited: RAAS blockade, BP target, statin when CV risk qualifies (this man may not meet PBS “high risk” thresholds despite family history), and SGLT2 inhibition for CKD — but his eGFR is not low enough to match many trial/PBS-style CKD criteria discussed on stage. SGLT2 for this phenotype may be off-label in Australia even when global guidelines feel persuasive.

GLP-1 receptor agonists (e.g. semaglutide 2.4 mg for obesity) may be on-label for weight (patient pays / access rules apply) but kidney outcome trials like FLOW were in diabetes. Observational/SURMOUNT-era signals in non-diabetes suggest less new albuminuria/CKD with substantial weight loss — biologically plausible “knock-on” kidney preservation, not a cure of the primary kidney disease.

Dual approach debated: GP leans metabolic syndrome (GLP-1 first); diabetes/kidney physician would also claim CKD and add SGLT2 if willing to use off-label, while banging on nephrology’s door with documented rapid decline. “The scariest thing is seeing a sick young person” — preserve whatever eGFR 65 he still has for the next 40 years.

What this means in clinic

1. Repeat eGFR/UACR to confirm chronicity (exclude AKI), then graph the slope.
2. Map real-world BP (ABPM/home), including night and triggers like vaping.
3. Do not dismiss green heat-map squares in young adults — compare to age-expected GFR.
4. Treat metabolic syndrome aggressively, but do not assume obesity alone explains low eGFR.
5. Know TGA/PBS vs guideline gaps for SGLT2/GLP-1; document shared decisions if off-label.
6. Advocate for nephrology review when decline is rapid — even if health pathways are rigid.

Take-home messages

• Early aggressive management in younger people is the headline — stop the slide into failure while they still have decades ahead.
• Trajectory (>~3 mL/min/year or ~10 mL over three years) outweighs a single reassuring heat-map colour.
• BP control is necessary but not sufficient; nocturnal coverage and true out-of-clinic BP matter.
• MASLD is a cardiometabolic warning light for heart, brain, and kidney — not only a liver problem.
• Preserve residual nephrons with metabolic unloading (weight, fats, glucose, BP); albuminuria can improve without “growing back” GFR.
• Drug access and labels in Australia may lag global CKD guidance — that tension was explicit in the seminar.

All Dr Kotha CPD pages · ckd-diabetes-young.drkotha.com