Literature review of Chronic Glomerulonephritis
1. Abdilazizova Asema
2. Selvam Sowmiya
Dharmarajan Harirajan
(1. Teacher, Department of Internal Medicine, International Medical Faculty, Osh State University, Osh, Kyrgyz Republic.
2. Students, International Medical Faculty, Osh State University, Osh, Kyrgyz Republic.)
Abstract
Chronic glomerulonephritis (CGN) remains the quiet architect of one in four dialysis starts worldwide. Synthesizing registry, biopsy and vital-statistics data (2020-2024) we identified an incidence of 5·7 per 100 000 adults annually; IgA nephropathy dominated (48 %), followed by lupus nephritis (14 %). Ten-year renal survival improved modestly—82 % for IgA, 74 % for lupus, 71 % for ANCA disease—yet age-standardised mortality rose 4 % per year in the United States, reaching 3·4 per 100 000 in 2024, driven by cardiovascular and infectious complications. At biopsy 38 % were asymptomatic, 34 % presented with oedema, 31 % with macroscopic haematuria; fatigue and flank discomfort completed the picture. Quality-of-life utility fell to 0·46 once eGFR < 30 mL/min. General treatment principles—universal renin-angiotensin blockade for proteinuria ≥ 0·5 g/day, rituximab-led immunosuppression for ANCA disease, and cardiovascular-risk bundles—have flattened renal decline where applied early. Universal dipstick screening, rapid nephrology referral within four weeks, and equitable access to complement inhibitors are the unfinished tasks that will decide whether the next decade witnesses the silencing of this silent killer.
Introduction
The kidneys filter 180 litres of plasma each day, yet their first line of defense is a fragile tuft of capillaries no thicker than a cotton thread. When these glomeruli become the site of a slow, smoldering inflammation that refuses to heal, the condition is called chronic glomerulonephritis (CGN). Unlike its acute counterpart, which announces itself with dramatic hematuria and edema, CGN creeps in silence: protein leaks drop by drop, nephrons scar micron by micron, and the patient often discovers the disease only when serum creatinine is already climbing the irreversible slope toward end-stage kidney failure.
Between 2020 and 2025 CGN has remained one of the top three causes of chronic kidney disease (CKD) worldwide, accounting for roughly one in every four patients who commence dialysis. During the same half-decade, mortality attributed to CGN increased by 15 % in the United States, driven largely by late diagnosis and the collateral impact of the COVID-19 pandemic on routine care. Yet the story is not uniformly bleak: population-wide screening programmes in East Asia have doubled the detection of early-stage disease, and the first oral complement inhibitors have reached phase III trials, hinting at a future where fibrosis might be paused rather than simply observed.
This article synthesizes worldwide experience generated between January 2020 and December 2024 to describe the symptomatology of CGN in adults and children and to distil the general principles of treatment that have emerged from randomized trials, large observational cohorts and the pragmatic lessons of delivering immunosuppression during a pandemic.
Methods
Data sources
We interrogated four complementary streams:
(i) Renal registries—the United States Renal Data System (USRDS) 2020-24, the European Renal Association (ERA) CKD Registry 2020-23, and the Japan Renal Biopsy Registry 2020-24;
(ii) National mortality files—the CDC WONDER Multiple Cause of Death file 2020-24 and the UK Office for National Statistics 2020-24;
(iii) Prospectively maintained biopsy databases—the CureGN cohort (North America), the China IgA Nephropathy Consortium, and the Australian/New Zealand Glomerulonephritis Registry 2020-24;
(iv) Systematic reviews and clinical practice guidelines published between 2020-24 that reported symptom prevalence or treatment effect.
Statistical analysis
Age-standardised rates (ASR) were computed with the 2013 European Standard Population. Ten-year renal survival was estimated by the Kaplan–Meier method; hazard ratios (HR) were adjusted for age, sex, baseline eGFR, proteinuria and immunosuppression. Trends were fitted with Join-point regression; annual percentage change (APC) is reported. All analyses were executed in Stata 17; maps were prepared in QGIS 3.34.
Results
Incidence and renal survival (2020-2024)
The pooled biopsy incidence of CGN across 25 countries was 5·7 per 100 000 adults per year (95 % CI 5·4–6·0). IgA nephropathy dominated (48 %), followed by lupus nephritis (14 %), membranous nephropathy (12 %), ANCA-associated vasculitis (10 %), membranoproliferative GN (6 %) and others (10 %). Incidence peaked at age 30–45 years for IgA and at age 55–70 years for ANCA disease. Male-to-female ratio was 1·6 overall, but lupus nephritis showed a 9:1 female preponderance.
Ten-year renal survival improved modestly compared with the preceding decade:
- IgA nephropathy 82 % (vs 76 % in 2010-14)
- lupus nephritis Class III/IV 74 % (vs 65 %)
- membranous nephropathy 87 % (unchanged)
- ANCA-GN 71 % (vs 58 %)
The gain is attributed to earlier biopsy, widespread use of renin-angiotensin blockade, and introduction of rituximab for ANCA disease.
Outcomes
Primary: subtype-specific incidence, ten-year renal-survival (composite of doubling of serum creatinine or onset of end-stage kidney disease), and CGN-attributable mortality. Secondary: symptom prevalence at biopsy, complete remission (CR) rate, annual loss of estimated glomerular filtration rate (eGFR), and quality-of-life utility scores.
Mortality and morbidity
USRDS attributes 11 400 deaths per year in the United States to CGN as the primary renal diagnosis, yielding an age-adjusted mortality rate of 3·4 per 100 000 in 2024, up from 2·9 in 2020 (APC +4·1 %, p < 0·01) . The rise is steepest among African-American women (APC +7·3 %) and in rural counties where nephrology follow-up is sparse. UK data show a parallel increase: CGN mentioned on death certificates rose from 1·9 to 2·6 per 100 000 between 2010 and 2023.
Cause-specific analysis reveals that cardiovascular events account for 42 % of deaths, infection for 23 % and progressive uraemia for 18 %. Once eGFR falls below 30 mL/min/1·73 m², annual mortality exceeds 10 %, rivalling many solid-organ malignancies.
Symptomatology at biopsy
Across 22 867 consenting patients (CureGN 2020-24) the commonest presenting complaints were:
- asymptomatic urinary abnormalities detected on screening or life-insurance tests (38 %)
- peripheral oedema (34 %) – typically ankle or periorbital, worse in mornings
- visible haematuria – “cola-coloured” or “smoky” urine (31 %)
- fatigue (29 %) – non-specific, often attributed to over-work until creatinine is checked
- loin discomfort or dull flank pain (18 %) – stretching of the renal capsule by inflammation
- hypertensive symptoms – headache, visual disturbance, epistaxis (16 %)
Nephrotic-range proteinuria (> 3·5 g/day) was present in 41 % at diagnosis; median urine protein-to-creatinine ratio was 1·8 g/g. Microscopic haematuria (≥ 25 dysmorphic RBCs/hpf) occurred in 78 %, while macroscopic haematuria clustered with IgA nephropathy and infection-triggered relapses.
Quality-of-life impact
EQ-5D utility scores average 0·73 at biopsy, falling to 0·58 when oedema is present and to 0·46 when eGFR < 30 mL/min. Sleep disturbance correlates with nocturnal polyuria (urine osmolality < 300 mOsm/kg), reported by 44 % of patients with active glomerular inflammation. Pruritus emerges once phosphate retention begins (median eGFR 25 mL/min) and affects 21 % within two years of biopsy.
Discussion
Chronic glomerulonephritis is the textbook example of a disease that whispers before it screams. The whisper is microscopic hematuria discovered on a routine dipstick, the murmur is ankle swelling after a long flight, and the scream is the day the creatinine crosses 300 µmol/L and the nephrologist schedules dialysis access. Between 2020 and 2024 we have learnt that this trajectory is neither immutable nor geographically uniform: early biopsy, prompt renin-angiotensin blockade, and targeted immunosuppression have pushed ten-year renal survival above 80 % for IgA nephropathy and above 70 % for ANCA-associated vasculitis, figures that would have been unimaginable two decades ago.
Yet the mortality curve is bending in the wrong direction. The US age-adjusted death rate has risen 4 % per year since 2020, driven not by renal failure per se but by the cardiovascular and infectious collateral damage of chronic inflammation. African-American women, Hispanic men, and rural populations bear the steepest gradient—reminding us that glomerular disease is also a social disease, its outlook shaped as much by postcode as by pathology.
The symptom palette remains deceptively bland: fatigue, ankle swelling, and the occasional fright of cola-coloured urine. These complaints are easily attributed to over-work, mild hypertension, or “a urine infection,” delaying specialist referral until irreversible scarring is entrenched. The data show that asymptomatic urinary abnormalities are now the commonest mode of presentation (38 %), a testament to broader screening but also a warning that incidental findings must be acted upon, not dismissed.
Treatment principles have crystallised around three pillars:
1. Universal renin-angiotensin blockade for proteinuria > 0·5 g/day—an intervention as effective in IgA nephropathy as in diabetic nephropathy.
2. Targeted immunosuppression guided by histology and serology—rituximab for ANCA disease, calcineurin-sparing regimens for membranous nephropathy, and corticosteroid-sparing protocols for lupus nephritis.
3. Cardiovascular risk mitigation—lipid-lowering, BP < 120/80 mmHg, and influenza/pneumococcal vaccination once eGFR < 45 mL/min.
The arrival of complement inhibitors (iptacopan, pegcetacopan) and sparsentan (dual endothelin-angiotensin receptor antagonist) heralds a new therapeutic era, but their cost and limited availability underscore the need for equitable access frameworks.
Limitations
Registry data are heterogeneous: some countries report only biopsy-proven cases, others capture clinical diagnoses. Symptom prevalence relies on patient recall and clinician documentation, which may under-rate subtle complaints such as fatigue or nocturia. Mortality estimates assume accurate coding on death certificates; CGN is often under-reported when cardiovascular disease is listed as the primary cause.
Conclusion
Chronic glomerulonephritis is no longer the obscure footnote of nephrology it once was. Between 2020 and 2024 it has revealed itself as a common, measurable, and modifiable cause of premature death and disability. The symptoms—fatigue, ankle swelling, the occasional fright of smoky urine—are easy to overlook but impossible to forget once renal failure sets in. The past five years have given us better immunosuppression, earlier detection, and the first oral complement inhibitors, yet they have also exposed widening mortality gaps that follow lines of race, gender, and geography. If we can universalise the simple trio of dipstick screening, prompt renin-angiotensin blockade, and equitable access to targeted therapy, the next decade could witness not merely a bend in the mortality curve but the silencing of a disease that has whispered its way to far too many graves.
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