IgA Nephropathy & CKD | Dr. Ni Zhaohu (Nephrology) | CMCS Shanghai

About Dr. Ni Zhaohu

Dr. Ni Zhaohu is Chief of Nephrology at Renji Hospital, Shanghai Jiao Tong University School of Medicine — one of China's foremost academic centres for kidney disease, chronic kidney disease management, and peritoneal dialysis. He is a nationally recognised leader in IgA nephropathy, glomerulonephritis, and renal replacement therapy, with particular expertise in precision immunosuppression, SGLT2 inhibitor-based renoprotective strategies, and automated peritoneal dialysis. Dr. Ni's practice is defined by the philosophy that the goal of nephrology is not merely to treat kidney disease — it is to preserve quality of life across the entire disease trajectory, from early glomerulonephritis through CKD progression to renal replacement therapy.

Case Overview

Mr. James Thornton, a 32-year-old British IT engineer based in Shanghai, presented with three days of macroscopic haematuria and foamy urine following acute tonsillitis two weeks prior. Serum creatinine was 280 μmol/L (eGFR 25 mL/min); 24-hour urine protein 3.5 g. Renal biopsy confirmed IgA nephropathy Oxford classification M1-E1-S1-T1 with cellular crescents in 3 of 16 glomeruli — a high-progression-risk profile with estimated five-year ESRD risk exceeding 50% without intervention. Dr. Ni Zhaohu designed an individualised induction regimen: moderate-dose prednisolone (0.5 mg/kg/day) combined with mycophenolate sodium, sacubitril/valsartan (ARNI), and early dapagliflozin (SGLT2 inhibitor) for non-glycaemic renoprotection. At four weeks, urine protein fell to 1.8 g/day and creatinine to 180 μmol/L. At three months, clinical remission was achieved: urine protein 0.9 g/day, creatinine 150 μmol/L, eGFR 38 mL/min. At one year, renal function is stable at CKD Stage 3b with no cushingoid side effects and no infections during immunosuppression.

Patient Background

• Name / Nationality: Mr. James Thornton (pseudonym) — British; IT engineer based in Shanghai
• Age / Sex: 32-year-old male
• Chief Complaint: Macroscopic haematuria and foamy urine for 3 days; elevated creatinine identified 1 day prior
• Precipitant: Acute tonsillitis 2 weeks prior — inadequately treated; IgA nephropathy classically flares 1–2 days after mucosal infection
• Prior History: Microscopic haematuria and proteinuria (0.8 g/day) on health check 3 years prior — not investigated further
• Admission: BP 150/95 mmHg; no peripheral oedema

Laboratory and Pathological Assessment

Laboratory

• Urinalysis: Dysmorphic red cells >80% — confirming glomerular origin; urine protein 3+
• 24-hour urine protein: 3.5 g — nephrotic-range proteinuria
• Renal function: Creatinine 280 μmol/L; eGFR 25 mL/min — AKI superimposed on CKD
• Serology: IgA 4.5 g/L (elevated); C3 normal; PLA2R, ANCA, ANA, dsDNA all negative — excluding membranous nephropathy, vasculitis, and lupus

Renal Ultrasound

• Bilateral kidneys normal size; corticomedullary differentiation preserved — normal size with acute creatinine rise supports active inflammatory disease; strong indicator for immunosuppressive intervention

Renal Biopsy

• Light microscopy: 16 glomeruli; 3 cellular crescents (18.75%); severe mesangial hypercellularity (M1); segmental sclerosis (S1); moderate tubulointerstitial damage (T1); endocapillary hypercellularity (E1)
• Immunofluorescence: IgA (+++) granular mesangial deposits; C3 co-deposition
• Oxford classification: M1-E1-S1-T1 with crescents — high-risk profile

Dr. Ni's diagnostic note: The Oxford classification is not a label. It is a treatment roadmap. M1 tells us the mesangial inflammation is active and will respond to immunosuppression. S1 and T1 tell us there is already chronic damage we cannot reverse — but we can stop it progressing. The crescents tell us the disease is in an acute phase right now. This patient needed treatment yesterday.

Clinical Decision Making

The patient had active crescentic disease with AKI — a narrow window for immunosuppressive intervention — combined with strong aversion to high-dose steroid side effects and the need to simultaneously address immunological injury and haemodynamic CKD progression drivers.

Dr. Ni Zhaohu's precision strategy: Not every crescent requires pulse methylprednisolone. For crescents below 50% and creatinine below 300, moderate-dose steroids combined with MMF achieve comparable remission rates with substantially lower infection risk. For a 32-year-old already immunologically stressed by recurrent tonsillitis, high-dose steroids add fuel to a fire. We use the minimum effective immunosuppression, add the renoprotective agents the evidence supports, and treat the infection source when the time is right.

Treatment Protocol

Phase 1 — Induction Immunosuppression

Prednisolone: 30 mg/day (0.5 mg/kg/day) — moderate-dose induction; planned taper over 6 months. High-dose pulse therapy deliberately avoided.

Mycophenolate sodium (MMF): 0.75 g twice daily, dose-adjusted for eGFR 25 mL/min. Suppresses T and B lymphocyte proliferation and mesangial IgA immune complex deposition. Selected over cyclophosphamide to preserve fertility in a young patient.

Prophylaxis: Co-trimoxazole (Pneumocystis); proton pump inhibitor; calcium and vitamin D.

Phase 2 — Renoprotective Foundation

Sacubitril/valsartan (ARNI): Titrated to maximum tolerated dose — targeting BP below 130/80 mmHg. Dual RAS blockade plus neprilysin inhibition reduces intraglomerular pressure and proteinuria more effectively than ACE inhibitor or ARB monotherapy.

Dapagliflozin 10 mg daily: Introduced at week 2. Non-glycaemic renoprotection based on DAPA-CKD trial evidence — 40% reduction in composite of eGFR decline, ESRD, and renal death in non-diabetic proteinuric CKD. Mechanism: tubuloglomerular feedback restoration; anti-inflammatory and anti-fibrotic effects independent of glucose lowering.

Dr. Ni's note: SGLT2 inhibitors used to be diabetes drugs. They are now kidney drugs. For a 32-year-old with a lifetime of kidney disease ahead of him, starting dapagliflozin now is not optional. It is the standard of care.

Phase 3 — Infection Source Management

Tonsillectomy: Planned at 6 months post-immunosuppression initiation. Tonsillar IgA1-producing plasma cells generate aberrantly glycosylated IgA1 forming mesangial immune complexes. Tonsillectomy reduces antigen stimulation and has been shown in Japanese and Chinese cohort studies to reduce proteinuria and haematuria recurrence. Timing critical — must follow immunosuppression stabilisation to minimise infection dissemination risk.

Treatment Response and Follow-up

• Week 4: Urine protein 1.8 g/day; creatinine 180 μmol/L; BP 130/80 mmHg — partial renal recovery confirmed
• Month 3: Urine protein 0.9 g/day (clinical remission); creatinine 150 μmol/L; eGFR 38 mL/min; MMF reduced to 0.5 g twice daily maintenance
• Month 6: Tonsillectomy uneventful; no post-operative flare; urine protein stable 0.7 g/day
• Month 12: CKD Stage 3b (eGFR 35 mL/min); urine protein 0.5–0.8 g/day; BP controlled; low-protein diet with ketoanalogue supplementation initiated
• Patient: Returned to full-time work; no cushingoid changes; no infections during immunosuppression

Expert Commentary — Dr. Ni Zhaohu

1. Oxford Classification as a Treatment Roadmap

The Oxford classification — M, E, S, T, C — is a clinical decision framework, not a research label. M1 and E1 indicate active immunosuppression-responsive lesions. S1 and T1 define the chronic damage baseline. C (crescents) signals acute necrotising injury requiring urgent intervention. In this patient, M1-E1 drove the immunosuppression decision; S1-T1 drove the renoprotective strategy; C3 drove the urgency. Reading the biopsy through the Oxford classification tells the clinician exactly which components are treatable, which are not, and how urgently treatment must begin.

2. Individualised Immunosuppression: Matching Intensity to Risk

The reflex to use high-dose pulse methylprednisolone for any IgA nephropathy with crescents is pattern-based, not evidence-based. The evidence supports high-dose steroids when crescent proportion exceeds 50% or creatinine rises rapidly above 300 μmol/L. Below those thresholds, moderate-dose prednisolone combined with MMF achieves comparable remission with substantially lower infection, metabolic, and bone density risk. This patient achieved clinical remission with no cushingoid side effects and no infections — the result of matching treatment intensity to disease risk, not applying a uniform protocol.

3. The SGLT2 Inhibitor Revolution in Non-Diabetic CKD

DAPA-CKD (2020) and EMPA-KIDNEY (2022) demonstrated significant reductions in eGFR decline, ESRD, and cardiovascular death in non-diabetic proteinuric CKD — a population that includes IgA nephropathy. The mechanism is independent of glucose lowering: tubuloglomerular feedback restoration reduces intraglomerular hypertension; direct anti-inflammatory and anti-fibrotic effects protect the tubulointerstitium. For a 32-year-old with decades of CKD trajectory ahead, early SGLT2 inhibitor initiation is now mandatory standard of care in proteinuric CKD regardless of diabetic status.

4. Peritoneal Dialysis: The Preferred Modality for Young, Active Patients

If disease progresses to ESRD despite optimal management, automated peritoneal dialysis (APD) is the preferred renal replacement modality. APD delivers dialysis during sleep, leaving the patient free during working hours — critical for a young professional. APD preserves residual renal function more effectively than haemodialysis, provides haemodynamic stability reducing cardiovascular risk, and avoids arteriovenous fistula and dialysis centre attendance burden. Renji Hospital's PD programme data demonstrate five-year survival equivalent to haemodialysis with superior quality-of-life scores. The goal is to delay dialysis as long as possible — and when necessary, to choose the modality that maximises the patient's ability to live a full and productive life.

How CMCS Shanghai Coordinated This Case

CMCS Shanghai supported Mr. Thornton from initial inquiry through twelve-month follow-up, including: pre-consultation review of external urinalysis, renal function, and health check records; specialist referral to Dr. Ni Zhaohu at Renji Hospital's Nephrology and Kidney Disease Institute; bilingual interpretation throughout all consultations, biopsy consent, and pathology review; coordination of renal biopsy, Oxford classification reporting, immunofluorescence, and electron microscopy; real-time biopsy result communication with bilingual Oxford classification explanation; ARNI titration and dapagliflozin prescription coordination; monthly renal function and urine protein monitoring with results translation to the patient's GP in the United Kingdom; tonsillectomy coordination at six months; dietary counselling for low-protein diet and ketoanalogue supplementation; and twelve-month surveillance protocol with direct liaison between Dr. Ni's team and the patient's nephrologist in London.

For international patients with IgA nephropathy, glomerulonephritis, or chronic kidney disease in Shanghai, Dr. Ni Zhaohu's team at Renji Hospital combines precision biopsy-guided immunosuppression, evidence-based renoprotection, and patient-centred long-term CKD management. CMCS ensures that expertise is accessible — in the patient's language, with overseas physicians informed at every treatment decision, from biopsy through long-term kidney preservation.

This case report is de-identified and published for educational purposes. All clinical details have been anonymized in accordance with patient privacy standards. CMCS Shanghai is a medical concierge service and does not provide direct medical care.