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GlomerulonephritisMANAGEMENT

GENITOURINARY AND REPRODUCTIVE PRESENTATIONS · 12 SECTIONS

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781 items

☷ Legend

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Cardiovascular Presentations71▾

Respiratory Presentations52▾

Neurological Presentations83▾

Gastrointestinal Presentations74▾

Genitourinary and Reproductive Presentations48▾

Acute Kidney Injury (ATN)Acute Kidney Injury (Post-renal)Acute Kidney Injury (Pre-renal)Amniotic Fluid Embolism Balanitis Bladder Rupture Breast Abscess Cystitis Dialysis access complications Ectopic pregnancy Epididymitis Glomerulonephritis Hematuria (gross)Hydrocele Interstitial Cystitis Mastitis Mittelschmerz Nephrolithiasis Nephrotic Syndrome Flare Nutcracker Syndrome Orchitis Ovarian Cyst Rupture Ovarian hyperstimulation syndrome Ovarian torsion Paraphimosis Pelvic Congestion Syndrome Pelvic Inflammatory Disease (PID)Peritoneal dialysis peritonitis Phimosis Priapism Prostatitis Pyelonephritis Renal laceration Renal transplant complications and rejection Ruptured ovarian cyst Testicular torsion Torsion of Appendix Testis Tubo-ovarian abscess Ureteral Rupture Urethritis Urinary Retention Urinary tract infection (uncomplicated)Urolithiasis (renal colic)Vaginal bleeding (non-pregnant)Vaginitis (Bacterial)Vaginitis (Candidal)Varicocele Vulvovaginal Hematoma

Infectious Disease Presentations148▾

Trauma Presentations89▾

Toxicologic Presentations80▾

Psychiatric Presentations26▾

Musculoskeletal and Rheumatologic Presentations96▾

Dermatology Presentations23▾

Environmental and Exposure Presentations27▾

Hematologic and Oncologic Presentations36▾

Pediatric-Specific Presentations19▾

Endocrine and Metabolic Presentations45▾

ENT and Maxillofacial Presentations27▾

Ophthalmologic Presentations19▾

Obstetric Presentations23▾

Systemic and Miscellaneous Presentations17▾

01Approach to the Critical Patient/attcp52

Immediate priorities

›Renal emergency recognition

›RPGN pattern: loss of kidney function over days to weeks

›Oliguria or anuria at presentation

›Rising creatinine with active urinary sediment

›Pulmonary-renal syndrome

›Hemoptysis plus AKI

›Anti-GBM disease or ANCA vasculitis until proven otherwise

›Hypertensive emergency with end-organ damage

›Encephalopathy, seizures, or flash pulmonary edema

›SBP >180 mmHg with neurologic symptoms

›If RPGN suspected, initiate urgent serologic workup and nephrology consult before biopsy

›Empiric treatment may be warranted before biopsy results return

›Every hour of delay worsens irreversible nephron loss

Hemodynamic stabilization

›Airway and volume assessment

›IV access x2, continuous monitoring

›Arterial line if hypertensive emergency

›Foley catheter for accurate hourly urine output

›Volume overload management

›IV furosemide 40-80 mg IV; higher doses if pre-existing CKD

›Fluid and sodium restriction

›Hypertensive emergency treatment

›IV nicardipine 5-15 mg/hr titrated to target

›IV labetalol 20 mg IV bolus, repeat every 10 minutes to 80 mg total

›Avoid nitroprusside in setting of renal failure

›Hyperkalemia management

›Calcium gluconate 1 g IV for membrane stabilization if ECG changes

02History/hx59

Presenting symptoms

›Core urinary symptoms

›Hematuria

›Gross (cola-colored, tea-colored, smoky) versus microscopic

›Clot-free hematuria favors glomerular origin

›Onset timing and duration

›Decreased urine output

›Oliguria (< 400 ml/day) or anuria suggests RPGN

›Rapid decline over days to weeks is a renal emergency

›Foamy urine indicating significant proteinuria

›Periorbital edema worse in the morning

›Facial edema distinguishes nephritic/nephrotic from cardiac edema

›Weight gain over days to weeks

Preceding events and exposures

›Infection history

›Pharyngitis or skin infection 1-3 weeks prior (post-streptococcal GN)

›10-14 day latency period for pharyngitis

›3-6 week latency for impetigo

›Synpharyngitic hematuria within 1-2 days of URI suggests IgA nephropathy

›Ongoing infection: endocarditis, abscess, ventriculoatrial shunt infection

›Recent travel to endemic areas for hepatitis B/C, HIV, malaria, schistosomiasis

›Medication history

›Hydralazine: most common drug-associated ANCA-GN; risk increases with >200 mg/day

›NSAIDs: can cause minimal change disease, membranous nephropathy, or interstitial nephritis

›Penicillamine, gold salts: membranous nephropathy

›Immune checkpoint inhibitors and anti-VEGF agents: thrombotic microangiopathy

›Levamisole-adulterated cocaine: ANCA vasculitis

›OTC supplements and skin-lightening creams containing mercury

03Physical Exam/exam42

Vital signs

›Blood pressure assessment

›Hypertension: often present; SBP >140 mmHg common

›Hypertensive urgency versus emergency distinction

›Fundoscopic changes if hypertensive emergency suspected

›Tachycardia and tachypnea suggesting volume overload or sepsis

›Fever raising concern for infectious etiology

›Oxygen saturation; desaturation with pulmonary hemorrhage

Volume status assessment

›Fluid overload signs

›Periorbital edema, peripheral pitting edema, anasarca

›Degree of edema grading (1+ to 4+)

›Weight gain from fluid retention

›Jugular venous distension

›JVP elevation >4 cm above sternal angle

›Abdominojugular reflex

›Pulmonary crackles and reduced air entry from pulmonary edema

›S3 gallop on cardiac auscultation

›New or changed cardiac murmur raising concern for endocarditis

Skin and mucocutaneous findings

›Vasculitis and autoimmune signs

›Palpable purpura: non-blanching, raised, lower extremities

›IgA vasculitis (Henoch-Schonlein purpura) in children

›Cryoglobulinemia in adults

›Malar rash sparing nasolabial folds: SLE

›Livedo reticularis: antiphospholipid syndrome

›Skin ulcers and nail-fold infarcts: systemic vasculitis

›Janeway lesions and Osler nodes: endocarditis

04Differential Diagnosis/ddx46

Life-threatening diagnoses

›Renal emergencies

›Rapidly progressive GN (RPGN): crescentic GN on biopsy

›ICD-10: N01 (rapidly progressive nephritic syndrome)

›Type I: anti-GBM disease (linear IgG on immunofluorescence)

›Type II: immune-complex GN (granular deposits on immunofluorescence)

›Type III: pauci-immune ANCA-associated (negative or scant immunofluorescence)

›Anti-GBM disease (Goodpasture syndrome)

›ICD-10: M31.0

›Pulmonary hemorrhage in ~60% of cases

›Linear IgG deposits along glomerular basement membrane

›ANCA-associated vasculitis

›Granulomatosis with polyangiitis (GPA, Wegener): PR3-ANCA positive

›Microscopic polyangiitis (MPA): MPO-ANCA positive

›Eosinophilic GPA (EGPA): MPO-ANCA positive, asthma, eosinophilia

Primary glomerulonephritides

›IgA nephropathy

›Most common GN worldwide

›ICD-10: N02.8

›Mesangial IgA deposits on immunofluorescence

›Synpharyngitic hematuria within 1-2 days of URI

›Distinguishes from 2-week latency of post-streptococcal GN

›20-40% progress to ESKD over 20 years without treatment

›Post-infectious GN (post-streptococcal)

›ICD-10: N00.8

›Pharyngitis 10-14 days prior; impetigo 3-6 weeks prior

›Excellent prognosis in children; worse in adults and elderly

05Laboratory Tests/lt70

Urine studies

›Urinalysis with microscopy

›Dysmorphic RBCs: >25% acanthocytes suggests glomerular origin

›Sensitivity 52-82% for glomerular disease

›Phase contrast microscopy preferred

›RBC casts: pathognomonic for GN

›Sensitivity low but highly specific

›Careful microscopy within 2 hours of voiding

›Granular and muddy brown casts: acute tubular injury

›WBC casts: interstitial nephritis or pyelonephritis

›Proteinuria quantification

›Spot urine protein-to-creatinine ratio (mg/mg): acceptable for initial assessment

›Nephrotic range: >3.5 g/g (>3.5 g/day)

›Subnephrotic: 0.15-3.5 g/g

›24-hour urine collection preferred for accurate quantification

›Urine albumin-to-creatinine ratio for monitoring CKD

Kidney function and electrolytes

›Serum creatinine and eGFR

›CKD-EPI formula for eGFR estimation

›Trending creatinine over hours to days to detect RPGN pattern

›Cystatin C-based eGFR if muscle mass is abnormal

›BUN-to-creatinine ratio: >20:1 suggests pre-renal component

›Electrolytes: sodium, potassium, bicarbonate, chloride

›Hyperkalemia: risk increases with eGFR <30 ml/min/1.73m2

›Metabolic acidosis: bicarbonate <22 mmol/l in AKI

›Serum phosphate and calcium: hyperphosphatemia and hypocalcemia in AKI

Serologic workup

›Complement levels

›C3 and C4

›Low C3: post-infectious GN, MPGN, SLE, cryoglobulinemia

›Low C4 with normal C3: cryoglobulinemia, SLE early

›Normal complement: IgA nephropathy, ANCA vasculitis, anti-GBM disease

›CH50: total hemolytic complement (global complement activation)

›ANCA panel

›c-ANCA/PR3-ANCA: GPA sensitivity 90% in active systemic disease

›Specificity 98% for ANCA vasculitis

›Both ELISA and indirect immunofluorescence recommended

›p-ANCA/MPO-ANCA: MPA, EGPA, drug-induced ANCA vasculitis

›Hydralazine: p-ANCA/MPO positive in 98% of drug-induced cases

›Anti-GBM antibody

›Sensitivity 90-95% for anti-GBM disease

›ELISA or indirect immunofluorescence on primate kidney substrate

›30% of anti-GBM disease patients also have ANCA (double-positive)

›If positive, initiate treatment before biopsy confirmation

›ANA and anti-dsDNA

›ANA sensitivity >95% for SLE but low specificity

›Anti-dsDNA: specificity 97% for SLE; correlates with disease activity

›Anti-Sm: highly specific for SLE (~25% sensitivity)

›Antiphospholipid antibodies: anticardiolipin, anti-beta2-glycoprotein I, lupus anticoagulant

Infection workup

›Streptococcal testing

›Anti-streptolysin O (ASO) titer: positive in 80% of post-pharyngitis GN

›Anti-DNase B: more sensitive for skin infection-associated GN

›Streptococcal infection confirmed in 95% if both tests used together

›Throat culture if active pharyngitis

›Blood cultures if endocarditis or sepsis suspected

›Viral serology

›Hepatitis B surface antigen and surface antibody

›Hepatitis C antibody and viral load

›HIV antibody and antigen

›Cryoglobulins (type I, II, III): hepatitis C most common cause of type II

Hematologic studies

›Complete blood count

›Anemia: chronic disease or microangiopathic hemolytic anemia

›Peripheral smear for schistocytes (TMA/TTP/HUS)

›LDH and haptoglobin for hemolysis assessment

›Thrombocytopenia: SLE, TTP/HUS, ANCA vasculitis

›Leukocytosis: infection-related GN or vasculitis

›Coagulation studies

›INR and PTT: baseline before plasma exchange or biopsy

›ADAMTS13 activity if TTP suspected

›Serum protein electrophoresis and urine protein electrophoresis

›Free light chains (kappa and lambda ratio) for monoclonal Ig-associated GN

›If positive, bone marrow biopsy for monoclonal Ig-associated GN

›LDH, uric acid, phosphate: tumor lysis syndrome consideration in malignancy-related GN

06Diagnostic Tests/dt112

Scoring Systems

›Clinical severity stratification

›Mild GN

›Isolated microscopic hematuria plus or minus subnephrotic proteinuria

›Preserved GFR (eGFR >60 ml/min/1.73m2)

›Outpatient nephrology referral appropriate

›Moderate GN (nephritic syndrome)

›Hematuria, proteinuria, edema, hypertension, mild AKI

›eGFR 30-60 ml/min/1.73m2

›Admission often required

›Severe/RPGN

›Rapidly declining GFR over days to weeks

›Oliguria, crescentic GN on biopsy

›eGFR <30 ml/min/1.73m2 and deteriorating

›Oxford Classification (MEST-C) for IgA nephropathy

›Mesangial hypercellularity (M0/M1)

›M1: >50% of glomeruli with mesangial hypercellularity

›Correlates with progression risk

›Endocapillary proliferation (E0/E1)

›Segmental glomerulosclerosis (S0/S1)

›Tubular atrophy/interstitial fibrosis (T0/T1/T2)

›Crescents (C0/C1/C2)

›ISN/RPS Lupus Nephritis Classification

›Class I: minimal mesangial; Class II: mesangial proliferative

›Classes I/II: generally good prognosis

›Treatment: hydroxychloroquine, supportive

›Class III: focal proliferative; Class IV: diffuse proliferative

›Classes III/IV: highest risk for ESKD

›Treatment: glucocorticoids plus mycophenolate or cyclophosphamide

›Class V: membranous; Class VI: advanced sclerosis

›ANCA disease activity scoring

›BVAS (Birmingham Vasculitis Activity Score): tracks disease activity

›Used to guide induction and maintenance therapy decisions

›VDI (Vasculitis Damage Index): tracks cumulative damage

Kidney Biopsy

›Indications and timing

›Definitive diagnosis in most cases of GN requiring immunosuppression

›Required for lupus nephritis classification

›Required for primary GN diagnosis and prognosis

›Exceptions: delay if clinical diagnosis compelling (anti-GBM, severe ANCA) and treatment cannot wait

›Also defer in active uncontrolled infection

›Correct coagulopathy first (INR <1.5, platelets >80 x10^9/l)

›Urgency: within 24-48 hours for RPGN

›Light microscopy findings

›Crescents: RPGN pattern

›Cellular crescents: acute (may be reversible)

›Fibrous crescents: chronic (irreversible)

›Percentage of glomeruli with crescents correlates with prognosis

›Mesangial proliferation: IgA nephropathy, post-infectious GN

›Endocapillary proliferation with subepithelial humps: post-streptococcal GN (starry sky)

›Membranous changes: membranous nephropathy, lupus Class V

›Immunofluorescence patterns

›Linear IgG along GBM: anti-GBM disease (pathognomonic)

›Granular IgG/IgM/C3: immune-complex GN (SLE, post-infectious, MPGN)

›Mesangial IgA: IgA nephropathy and IgA vasculitis

›Negative or pauci-immune: ANCA vasculitis

Scoring Systems (continued 1)

›Kidney disease staging

›AKI staging by KDIGO criteria

›Stage 1: creatinine rise 1.5-1.9x baseline or increase 26.5 micromol/l

›Stage 2: creatinine rise 2.0-2.9x baseline

›Stage 3: creatinine rise >3x baseline, initiation of RRT, or eGFR <35 ml/min if age <18

›CKD staging by eGFR (G1-G5) and albuminuria (A1-A3)

›Used for prognosis and risk stratification after acute episode

›KFRE (Kidney Failure Risk Equation): 2-year and 5-year risk of ESKD

MRI

›Renal MRI applications

›Limited role in acute GN diagnosis; primarily used for structural assessment

›No radiation: preferred in pregnancy or young patients requiring repeated imaging

›Gadolinium contraindicated with eGFR <30 ml/min/1.73m2 (nephrogenic systemic fibrosis risk)

›Renal cortical signal on diffusion-weighted imaging

›ADC values correlate with degree of inflammation and fibrosis

›Research application for non-invasive fibrosis assessment

›MRI angiography for renal artery assessment

›Renovascular hypertension as contributor to acute presentation

›Fibromuscular dysplasia in young women

›Pulmonary MRI in pulmonary-renal syndrome

›Pulmonary hemorrhage: bilateral ground-glass opacities

›Avoids radiation in patients requiring serial imaging

›CT abdomen and pelvis with contrast

›Indications in GN setting

›Rule out obstructive uropathy before attributing AKI to GN

›Assess for bilateral renal involvement versus unilateral process

›Identify peri-nephric collections or abscess

›Findings in acute GN

›Enlarged, edematous kidneys with poor corticomedullary differentiation

›Perinephric fat stranding

›Preserved cortical enhancement distinguishes GN from cortical necrosis

›CT chest for pulmonary-renal syndrome

›Ground-glass opacities: diffuse alveolar hemorrhage

›Bilateral involvement with perihilar distribution

›Distinguish from pulmonary edema (cardiomegaly, pleural effusions)

›CT sinuses: destructive sinusitis in GPA

›Bone erosion and septal perforation

›Pan-sinusitis pattern

›Contrast considerations

›Avoid iodinated contrast if creatinine rising rapidly

›Risk of contrast nephropathy lower than previously thought but minimize dose

›Hydration with isotonic saline if contrast required

Ultrasound

›Renal ultrasound (first-line imaging)

›Indications: all patients with AKI and suspected GN

›Rule out obstructive uropathy (hydronephrosis)

›Assess kidney size: enlarged (acute GN) versus small (chronic CKD)

›Cortical echogenicity: increased echogenicity suggests chronicity

›Findings in acute GN

›Normal or enlarged kidneys (>12 cm pole-to-pole length)

›Increased cortical echogenicity relative to liver/spleen

›Loss of corticomedullary differentiation in severe cases

›Renal Doppler

›Resistive index (RI) >0.7 suggests elevated intrarenal resistance

›RI >0.8 associated with poor renal recovery

›Rule out renal vein thrombosis in nephrotic syndrome

›Cardiac point-of-care ultrasound

›LV function and wall motion for hypertensive emergency assessment

›Pericardial effusion in uremic pericarditis

›Volume status assessment: IVC collapsibility index

07Disposition/dispo43

Admission indications

›Mandatory admission criteria

›RPGN or rapidly declining renal function

›Daily creatinine monitoring required

›Urgent biopsy coordination

›Pulmonary-renal syndrome with hemoptysis

›ICU level care for respiratory compromise

›Plasma exchange coordination

›Severe hypertension or hypertensive emergency

›IV antihypertensive therapy required

›Continuous blood pressure monitoring

›AKI requiring or potentially requiring dialysis

›Refractory hyperkalemia >6.5 mmol/l

›Severe metabolic acidosis pH <7.1

›Significant volume overload requiring IV diuretics

›Need for urgent plasma exchange (anti-GBM disease)

›Children with significant edema, severe hypertension, or AKI

Level of care determination

›ICU admission

›Pulmonary hemorrhage with respiratory compromise

›SpO2 <92% despite supplemental oxygen

›Requiring mechanical ventilation

›Refractory hypertensive emergency despite IV therapy

›Hemodynamic instability requiring vasopressors

›Active dialysis management with hemodynamic instability

›Nephrology ward admission

›New-onset nephritic syndrome with stable renal function pending serologic results

›Initiation of immunosuppression requiring monitoring

08Treatment/t116

Acute supportive care

›Volume and electrolyte management

›Sodium restriction: <2 g/day (<90 mmol/day) for edema and blood pressure control

›KDIGO 2021 guideline recommendation

›Fluid restriction in oliguric patients

›Diuresis for volume overload

›Furosemide IV 40-80 mg; higher doses (80-240 mg) with significant CKD

›May require continuous infusion 10-40 mg/hr if bolus ineffective

›Monitor urine output response at 2 hours

›Combination with thiazide (chlorothiazide 250-500 mg IV) for diuretic resistance

›Dietary protein restriction: 0.8-1.0 g/kg/day

›Avoid high-protein diets which worsen proteinuria

›Plant-based protein sources preferred when possible

›Hypertension management

›Acute severe hypertension (inpatient)

›Nicardipine IV 5-15 mg/hr titrated to target SBP <160 mmHg

›Titrate by 2.5 mg/hr every 5-15 minutes

›Maximum 15 mg/hr

›Labetalol IV 20 mg bolus, repeat every 10 minutes

›Maximum cumulative bolus dose 300 mg

›Continuous infusion 1-2 mg/min if needed

›Hydralazine IV 10-20 mg every 4-6 hours as alternative

›Long-term blood pressure control

›ACEi or ARB at maximally tolerated doses: first-line for all GN with proteinuria

›Target SBP <120 mmHg per KDIGO 2021

›Reduces proteinuria and slows CKD progression

›SGLT2 inhibitors (dapagliflozin, empagliflozin): added benefit in CKD

›Reduce proteinuria and GFR decline independent of glucose control

›DAPA-CKD and EMPA-KIDNEY trial evidence

Disease-specific immunosuppression

›ANCA-associated vasculitis induction

›Rituximab plus glucocorticoids: preferred first-line induction

›Rituximab 375 mg/m2 IV weekly x 4 doses or 1 g IV x 2 doses (2 weeks apart)

›RAVE and RITUXVAS trials support equivalence to cyclophosphamide

›Preferred over cyclophosphamide in relapsing disease and elderly

›Methylprednisolone 500-1000 mg IV daily x 3 days (pulse)

›Then prednisone 1 mg/kg/day (maximum 80 mg/day)

›Taper over 4-6 months to target prednisone 5-7.5 mg/day by 6 months

›Cyclophosphamide alternative for induction

›IV cyclophosphamide 15 mg/kg (maximum 1.2 g) every 2-3 weeks x 6 pulses

›Reduce dose by 25% if age >60 or eGFR <20 ml/min/1.73m2

›Mesna uroprotection with each dose

›Oral cyclophosphamide 2 mg/kg/day for up to 3-6 months

›Monitor CBC weekly (hold if WBC <4 x10^9/l or neutrophils <2 x10^9/l)

›Plasma exchange in severe ANCA vasculitis

›PEXIVAS trial: plasma exchange did not reduce ESKD or death at 7 years

›Current guidance: reserved for dialysis-dependent AKI or DAH

›60 ml/kg exchange per session (minimum 4 liters)

›Maintenance therapy after remission

›Rituximab 500 mg IV every 6 months x 2 years (preferred)

›Azathioprine 2 mg/kg/day as alternative

›Anti-GBM disease treatment

›Plasma exchange daily x 14 days or until anti-GBM antibody undetectable

›4-liter exchanges with 5% albumin replacement

›Fresh frozen plasma if active pulmonary hemorrhage

›Initiate before biopsy confirmation if high clinical suspicion

›Cyclophosphamide 2-3 mg/kg/day (maximum 200 mg/day) x 2-3 months

›Reduce by 25% if age >55 or creatinine >500 micromol/l

›Monitor CBC weekly

›Prednisone 1 mg/kg/day (maximum 60-80 mg/day)

›Taper by 10 mg every 2 weeks after plasma exchange complete

›Total duration 6-9 months

›Prognosis: patients presenting on dialysis with >50% crescents rarely recover renal function

›Exception: those with concurrent ANCA positivity may recover

›Lupus nephritis Class III/IV treatment

›Glucocorticoids plus mycophenolate mofetil (MMF): first-line induction

›MMF 2-3 g/day (target trough 1.5-3 mg/l if monitored)

›ALMS trial: MMF non-inferior to cyclophosphamide for induction

›Preferred in women of childbearing potential

›Methylprednisolone 500-1000 mg IV x 3 days then prednisone 0.5-1 mg/kg/day

›Voclosporin or tacrolimus: add-on therapy for refractory disease

›Voclosporin 23.7 mg twice daily (AURORA trial)

›Combination with MMF and low-dose steroids

›Belimumab (anti-BLYS): FDA-approved add-on for active lupus nephritis

›10 mg/kg IV monthly x 3 doses then every 4 weeks

›BLISS-LN trial: reduced renal and overall flares

›Hydroxychloroquine background therapy: all lupus nephritis patients

›200-400 mg/day; target 5 mg/kg/day (weight-based to reduce retinal toxicity)

›Maintenance therapy

›MMF 1-2 g/day (preferred) or azathioprine 2 mg/kg/day

›IgA nephropathy treatment

›Optimized supportive care: first and ongoing treatment

›RASi (ACEi or ARB) at maximal tolerated dose

›Target proteinuria <1 g/day

›KDIGO 2021: Class I recommendation

›Sodium restriction <2 g/day

›Blood pressure target <120/70 mmHg

›SGLT2 inhibitors: added benefit with CKD and proteinuria

›Dapagliflozin 10 mg/day: DAPA-CKD trial (40% reduction in progression)

›Empagliflozin 10 mg/day: EMPA-KIDNEY trial

›Corticosteroids for persistent proteinuria >1 g/day despite 3 months supportive care

›Oral prednisolone 0.5-1 mg/kg/day (maximum 60 mg/day) tapered over 6 months

›NefIgArd trial: targeted release formulation of budesonide (Nefecon) effective

›16 mg/day Nefecon x 9 months reduced proteinuria vs placebo

›Significant risk: infection (especially pneumocystis pneumonia prophylaxis)

›Sparsentan (dual endothelin and angiotensin receptor antagonist)

›FDA-approved 2023 for IgA nephropathy

›400 mg/day: PROTECT trial showed superior proteinuria reduction vs irbesartan

›Fish oil: inconclusive evidence; may be considered in mild IgA nephropathy

›Post-infectious GN treatment

›Primarily supportive care

›Antibiotics only if active streptococcal infection persists

›Penicillin V or amoxicillin x 10 days for active pharyngitis

›Does not alter GN course once established

›Volume management and antihypertensives as above

›Prognosis: excellent in children; 95% achieve complete remission

›Adults and elderly: less favorable, up to 25-40% develop CKD

›Avoid immunosuppression unless biopsy shows crescentic pattern

Adjunctive long-term management

›Cardiovascular risk reduction

›Statin therapy per CKD guidelines

›Cardiovascular disease risk 2.5x general population in primary GN

›KDIGO: statin or statin/ezetimibe for adults with CKD >50 years

›Smoking cessation

›Accelerates GN progression and associated with nodular glomerulosclerosis

›Weight optimization and regular aerobic exercise

›Anticoagulation in nephrotic syndrome

›Thromboembolism risk increased with proteinuria >3.5 g/day

›Prophylactic anticoagulation if albumin <20 g/l in membranous nephropathy

09Special Populations/sp80

Pregnancy

›Pregnancy in GN: key considerations

›Physiologic changes complicating assessment

›Physiologic GFR increase of 40-65% in pregnancy (creatinine normally falls to ~44-62 micromol/l)

›Physiologic proteinuria increase up to 300 mg/day in normal pregnancy

›Distinction from pre-eclampsia may be very difficult

›Pre-eclampsia versus GN distinction

›Pre-eclampsia: onset typically >20 weeks; resolves after delivery

›Active GN: onset may be any gestational age; active urinary sediment

›Renal biopsy relatively safe up to 28 weeks if diagnosis uncertain

›Maternal and fetal risks

›Increased risk of pre-eclampsia (2-7x baseline) in women with GN

›Preterm delivery, intrauterine growth restriction

›Higher risk with eGFR <40 ml/min/1.73m2 or proteinuria >1 g/day at conception

›Medication safety in pregnancy

›Safe or relatively safe

›Hydroxychloroquine: continue throughout pregnancy in lupus nephritis

›Class C; benefits generally outweigh risks; reduces lupus flares in pregnancy

›Azathioprine: relatively safe; used for maintenance lupus nephritis in pregnancy

›Dose 1-2 mg/kg/day; FDA category D but widely used

›Low-dose prednisone: acceptable; use lowest effective dose

›Low-dose aspirin (81 mg/day): reduces pre-eclampsia risk from 28 weeks

›Avoid or contraindicated in pregnancy

›ACEi/ARB: teratogenic in second and third trimesters (renal agenesis, limb defects)

›Discontinue before conception or immediately on diagnosis of pregnancy

›MMF: teratogenic (ear and limb defects); stop at least 6 weeks before conception

›Cyclophosphamide: teratogenic; avoid in first trimester

›SGLT2 inhibitors: insufficient data; generally avoided

Geriatric

›Epidemiology in elderly

›Infection-related GN increasingly affects elderly with comorbidities (Staphylococcus aureus, MRSA)

›Shift from streptococcal (children) to staphylococcal (elderly, diabetics) infection-related GN

›Outcomes significantly worse than in children

›ANCA vasculitis incidence peaks at 65-74 years

›Monoclonal immunoglobulin-associated GN: predominantly in patients >50 years

›Modified management approach

›Immunosuppression risks magnified

›Cyclophosphamide: reduce dose by 25-33% if age >60 or creatinine >300 micromol/l

›Infection risk markedly increased; PCP prophylaxis mandatory (trimethoprim-sulfamethoxazole DS 3x/week)

›Varicella-zoster vaccination before immunosuppression if possible

›Rituximab: preferred over cyclophosphamide in elderly due to lower infection risk

›Glucocorticoids: high risk of osteoporosis, hyperglycemia, neuropsychiatric effects

›Calcium 1000-1500 mg/day and vitamin D 800-1000 IU/day supplementation

›Bisphosphonate for bone protection with prolonged steroid use

›Drug dosing adjustments

›ACEi/ARB: start at lowest dose; monitor potassium and creatinine closely

›Creatinine rise of up to 20-30% acceptable with RASi initiation (not AKI)

›Furosemide: reduced sensitivity; higher doses often required

›Avoid NSAIDs entirely in elderly with any GN

›Comorbidity management

›Diabetes: worsens prognosis of infection-related GN

›Higher prevalence of cardiovascular disease complicating volume management

›Dialysis access planning earlier if trajectory suggests progression

Pediatrics

›Most common pediatric GN: post-streptococcal and IgA nephropathy

›Post-streptococcal GN peaks in children 2-10 years

›Excellent prognosis: 95% complete remission

›Creatinine normalizes within approximately 4 weeks

›Hematuria resolves within 3-6 months; microscopic hematuria may persist 2 years

›IgA vasculitis (Henoch-Schonlein purpura) in children

›Tetrad: palpable purpura, arthritis, abdominal pain, renal disease

›Renal involvement in 20-50%; usually mild and self-resolving

›Pediatric-specific assessment

›Blood pressure: must use age, sex, and height-specific norms (normative tables)

›Hypertension diagnosis requires >95th percentile on repeated measurements

›Hypertensive emergency: systolic BP >30 mmHg above 95th percentile

›Admission criteria in children

›Significant edema, severe hypertension, or AKI

›Inability to maintain adequate oral intake

›Concern for pulmonary edema or hypertensive emergency

›Pediatric dosing and treatment

›Furosemide: 0.5-2 mg/kg/dose IV (maximum 6 mg/kg/day)

›Amlodipine: 0.05-0.3 mg/kg/day PO for hypertension (maximum 10 mg/day)

›Hydralazine: 0.1-0.5 mg/kg/dose IV every 4-6 hours for acute severe hypertension

›Prednisone in pediatric nephrotic/nephritic: 2 mg/kg/day (maximum 60 mg/day) x 4-6 weeks

›Renal biopsy in pediatrics

›Indicated if steroid-resistant, atypical features, or progressive renal impairment

›Generally safe from age 3-4 years; ultrasound guidance mandatory

›Penicillin V 250 mg twice daily for 10 days if active streptococcal infection

›Does not alter course of established GN but eradicates nephritogenic strain

›Follow-up: AsPNA 2026 guidelines recommend serial monitoring for all children with infection-related GN

›Urinalysis and BP every 3-6 months for 2 years

›Referral to pediatric nephrology for all cases

10Background/b87

Epidemiology

›Global prevalence and incidence

›GN is the third leading cause of ESKD worldwide (after diabetes and hypertension)

›Accounts for approximately 10-15% of all ESKD cases in developed countries

›Higher proportion in developing countries (up to 30-40% of ESKD)

›IgA nephropathy: most common primary GN worldwide

›Prevalence 25-50 cases per 100,000 in developed countries

›Higher prevalence in Asian populations (up to 40% of all primary GN)

›20-40% progress to ESKD over 20 years without treatment

›Post-infectious GN

›Incidence 472,000 cases/year globally; 456,000 in developing countries

›Children account for 70% of cases globally

›In developed countries, shift to elderly adults with staph infections

›ANCA vasculitis

›Incidence 10-20 cases per million per year in Europe and North America

›Peaks at age 65-74 years; slight male predominance

›Anti-GBM disease

›Incidence 0.5-1 case per million per year

›Bimodal age distribution: young men (20-30 years) and older women (60-70 years)

›Lupus nephritis

›Affects 50-60% of patients with SLE

›Predominantly young women (age 15-45); higher incidence in African American and Hispanic populations

›Mortality and morbidity

›Cardiovascular disease risk 2.5x general population in primary GN

›Proteinuria independently accelerates atherosclerosis

›Hypertension and dyslipidemia contribute

›RPGN without treatment: 90% mortality within weeks to months

›ANCA vasculitis with treatment: 5-year survival approximately 70-80%

›Anti-GBM disease: renal survival depends on creatinine at diagnosis

›Creatinine <500 micromol/l: good renal outcomes with treatment

›Dialysis-dependent at presentation: <10% recover independent renal function

Pathophysiology

›Immunopathological mechanisms

›Immune-complex GN

›In situ immune complex formation (post-streptococcal, membranous nephropathy)

›Planted antigens (streptococcal neuraminidase alters IgG, complement activation)

›Subepithelial humps (post-streptococcal) or subendothelial deposits (lupus Class III/IV)

›Circulating immune complex deposition (lupus, cryoglobulinemia, endocarditis-associated)

›Complement activation via classical pathway (C1q, C4, C3, MAC formation)

›ANCA-associated (pauci-immune) GN

›Neutrophil-mediated glomerular injury without immune deposits

›ANCA activates primed neutrophils at endothelial surface

›Neutrophil degranulation releases proteases and reactive oxygen species

›Fibrinoid necrosis and crescent formation

›Complement alternative pathway amplification

›C5a and C5aR1 inhibitor (avacopan) targets this pathway

›Anti-GBM GN

›Autoantibodies against NC1 domain of alpha-3 chain of type IV collagen

›Cross-reactivity with pulmonary alveolar basement membrane causes pulmonary hemorrhage

›Linear IgG deposition triggers complement and neutrophil activation

›T-cell mediated injury also contributes

›C3 glomerulopathy

›Dysregulation of alternative complement pathway (C3 nephritic factor, factor H/I mutations)

›C3 deposits without significant immunoglobulin on immunofluorescence

›Dense deposit disease (DDD) and C3 glomerulonephritis (C3GN) subtypes

›Crescentic GN and RPGN mechanism

›Bowman space proliferation of parietal epithelial cells with monocyte influx

›Fibrin deposition in Bowman space triggers crescent formation

›Cellular crescents: potentially reversible with early immunosuppression

›Conversion to fibrous crescents: permanent loss of filtration surface

›Each glomerulus with crescent = irreversible loss of that nephron unit

›RPGN with >50% crescents: poor renal prognosis even with treatment

›GFR at presentation is strongest predictor of renal outcome

Therapeutic Considerations

›Evidence base for treatment

›Immunosuppression risks versus benefits

›Infection is leading cause of death in treated vasculitis and lupus nephritis

›Cyclophosphamide: lifetime dose limits (bladder cancer risk >25 g cumulative)

›PCP prophylaxis (trimethoprim-sulfamethoxazole DS 3x/week) for all patients receiving cyclophosphamide

›Rituximab has replaced cyclophosphamide in many settings (RAVE, RITUXVAS trials)

›Treatment of active infection before immunosuppression

›Infection-related GN: immunosuppression may worsen outcomes

›Endocarditis-associated GN: antibiotics and cardiac surgery if needed; avoid IS

›Complement inhibition: emerging therapy

›Avacopan (C5aR1 inhibitor): FDA-approved for ANCA vasculitis

›ADVOCATE trial: avacopan 30 mg twice daily non-inferior to prednisolone taper

›Superior remission maintenance at 52 weeks; allows steroid reduction

›Eculizumab (C5 inhibitor): refractory C3 glomerulopathy and aHUS

›Fibrosis prevention

›Early treatment reduces irreversible nephron loss

›RASi and SGLT2 inhibitors reduce progression independent of immunosuppression

›Anti-fibrotic targets (TGF-beta, pirfenidone) under investigation

›Biomarker monitoring

›Urinary protein creatinine ratio as treatment response biomarker

›Target <0.5 g/g for most GN types

›Lupus nephritis: complete renal response requires PCR <0.5 g/g with stable eGFR

›ANCA titers: rising titers may precede clinical relapse by weeks

›Not independently sufficient to justify treatment change

›Anti-GBM antibody: must become undetectable before stopping plasma exchange

›Complement levels: guide activity in lupus and complement-mediated GN

11Patient Discharge Instructions/pdi35

copy discharge instructions

›Discharge instructions for Glomerulonephritis

›What is glomerulonephritis?

›GN is inflammation of the kidney filters (glomeruli), which can cause blood and protein in the urine, high blood pressure, and reduced kidney function

›Many different causes exist; your doctor will explain which type you have

›Some forms are mild and resolve on their own; others require specific treatment

›Diet and lifestyle instructions

›Limit salt (sodium) to less than 2 grams per day (no added salt, avoid processed foods)

›Limit fluid intake if you have swelling or your doctor instructs you to do so

›Moderate protein intake: 0.8-1.0 g per kg of your body weight per day

›Avoid NSAIDs (ibuprofen, naproxen, aspirin for pain): these can worsen kidney function

›Avoid dehydration: take your medications with adequate water

›Weigh yourself daily: report a gain of more than 2 kg (4.4 lbs) in 48 hours to your doctor

›Medications

›Take all prescribed medications exactly as directed

›If prescribed blood pressure medications (ACE inhibitor or ARB), do not stop without calling your doctor

›If prescribed immunosuppressive medications (prednisone, mycophenolate, cyclophosphamide, rituximab), follow all monitoring instructions

›Do not take any new medications including vitamins and supplements without consulting your nephrologist

›Monitoring at home

›Check and record blood pressure daily if a home cuff is available

›Target blood pressure below 130/80 mmHg (your doctor may specify a different target)

›Note changes in urine color, amount, or foaminess

›Return to emergency room immediately for

›Emergency symptoms requiring immediate care

›Decreased or no urine output

›Cola-colored or bloody urine returning or worsening

›Rapid weight gain or markedly worsening leg swelling

›Severe headache, vision changes, or confusion (possible hypertensive emergency)

12References/r39

Guidelines and key sources

›Primary references

›Sethi S, De Vriese AS, Fervenza FC. Acute Glomerulonephritis. Lancet. 2022

›PubMed: 35461559

›Comprehensive review of GN pathophysiology and management

›KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases

›Kidney International 2021; comprehensive guidance for all GN subtypes

›Available at: kdigo.org/wp-content/uploads/2024/05/KDIGO-2021

›KDIGO 2024 Guideline for ANCA-Associated Vasculitis

›Kidney International 2024

›PubMed: S0085-2538(23)00744-5

›Sethi S, Haas M, Markowitz GS et al. Mayo Clinic/Renal Pathology Society Consensus Report on Pathologic Classification, Diagnosis, and Reporting of GN. JASN 2016

›PubMed: 26567243

›Key clinical trials

›RAVE trial (rituximab versus cyclophosphamide for ANCA vasculitis induction)

›NEJM 2010; rituximab non-inferior at 6 months for remission

›Superior in relapsing disease

›PEXIVAS trial (plasma exchange in ANCA vasculitis)

›NEJM 2020; plasma exchange did not reduce ESKD or death at 7 years

›Reserved for dialysis-dependent or pulmonary hemorrhage

›ADVOCATE trial (avacopan in ANCA vasculitis)

›NEJM 2021; avacopan non-inferior to prednisolone, superior at 52 weeks

›PROTECT trial (sparsentan in IgA nephropathy)

›NEJM 2023; superior proteinuria reduction versus irbesartan

›DAPA-CKD trial (dapagliflozin in CKD with proteinuria)

›NEJM 2020; 40% reduction in progression to ESKD

›NefIgArd trial (targeted-release budesonide for IgA nephropathy)

›NEJM 2023; Nefecon 16 mg/day significantly reduced proteinuria

Learn More: Glomerulonephritis→

Comprehensive Clinical Review

Structured, evidence-informed, long-form analysis for deeper understanding.

Evidence & Review

Reviewed by SymptomDx Medical Team · Last reviewed August 18, 2026

SymptomDx is an educational tool for medical professionals. It does not replace clinical judgment. Verify all clinical data and drug dosages with authoritative sources.