C1q Nephropathy

C1q nephropathy is a rare kidney disease. It affects the filters of the kidney called glomeruli. In this disease, the body’s immune system leaves a protein called C1q in the mesangium (the support tissue inside each glomerulus). Kidney specialists see this on a kidney biopsy using immunofluorescence: C1q staining is dominant or co-dominant in the mesangium. A key rule is that patients do not have clinical or blood test features of lupus (no lupus symptoms, negative lupus blood tests). So it is not lupus nephritis, even though the biopsy can look similar under the microscope. PMC+2ScienceDirect+2

C1q nephropathy is an uncommon kidney disease where a biopsy shows strong (“dominant”) deposits of a complement protein called C1q in the kidney’s filtering unit (the glomerulus), usually in the mesangium. People may have swelling, heavy protein in urine (nephrotic range), or findings that look like minimal-change disease or focal segmental glomerulosclerosis (FSGS). It is a clinicopathologic pattern rather than a single cause, so treatment is adapted from best practices for proteinuric glomerular diseases and case series. PMC+1

Doctors first recognized C1q nephropathy as a special pattern on biopsy, not a single uniform illness. It can show up with different light-microscopy patterns (for example, minimal change disease, focal segmental glomerulosclerosis (FSGS), or mesangial proliferative glomerulonephritis). The common feature is the strong C1q signal in the mesangium. AJKD+1

C1q nephropathy is a kidney disease where the immune system’s C1q protein (part of the complement system) sticks in the filtering units of the kidney (the glomeruli), mainly in the middle part called the mesangium. Doctors see this by special staining (immunofluorescence) on a kidney biopsy. Light microscopy (the usual microscope) can look normal or show patterns that mimic other diseases such as minimal-change disease (MCD), focal segmental glomerulosclerosis (FSGS), or a proliferative glomerulonephritis. Electron microscopy often shows deposits in the mesangium. It is diagnosed only when there is no clinical or blood-test evidence of lupus (SLE). PMC+2PMC+2

People can come with heavy protein in the urine (nephrotic syndrome), blood in urine (hematuria), or just abnormal urine tests. In children it can be a cause of nephrotic syndrome; in adults it is rarer. Response to steroids varies: some respond, but many—especially those with an FSGS pattern—do not respond well. PMC+2PMC+2

Other names

Doctors may also call it “C1q-dominant mesangial immune complex glomerulopathy,” “C1q-dominant glomerulonephritis,” or briefly “C1q GN.” These names all mean the same idea: kidney inflammation where C1q is the main or co-main immune deposit in the mesangium on biopsy, without evidence of lupus. Krcp Ksn+1

Types

1) Minimal-change–like type. The glomeruli look almost normal on light microscopy, but electron microscopy shows podocyte foot-process effacement, and immunofluorescence shows strong C1q in the mesangium. Patients often have nephrotic syndrome. PMC

2) FSGS-like type. Some glomeruli show scars (segments) typical of FSGS. This group tends to have heavier proteinuria and a poorer steroid response. PMC+1

3) Proliferative type. There are more cells in the glomerulus (mesangial or endocapillary proliferation). Proteinuria and hematuria are common. PMC

(These are patterns seen on biopsy—C1q nephropathy is defined by the C1q-dominant deposits, and the light-microscopy pattern can vary.) ScienceDirect

Causes

There is no single proven cause for all cases. Doctors think several mechanisms or conditions may be involved. Below are possible causes/associations reported in the medical literature; many cases are still idiopathic (no clear cause).

1. Idiopathic immune dysregulation. Many people have no identifiable trigger; their immune system simply forms mesangial immune deposits rich in C1q. PMC

2. Complement system over-activation. Extra activation of the classical pathway (where C1q acts) can drive deposits in the mesangium. WJNU

3. Viral infections (general). Case reports describe C1q-dominant deposits after viral illnesses, suggesting an infection-related immune-complex process. ResearchGate

4. Hepatitis viruses. Some immune-complex glomerulonephritides linked to hepatitis have complement-rich deposits; rare cases show C1q dominance. (Association; not universal.) PMC

5. HIV. Viral antigens can stimulate immune-complex formation; rare C1q-dominant patterns have been described. (Association varies by series.) PMC

6. Post-infectious states. After certain infections, immune complexes can lodge in glomeruli; a minority show strong C1q. PMC

7. Autoimmune tendency (non-lupus). Some patients have autoantibodies or immune activation without meeting lupus criteria; C1q deposits can still be present. WJNU

8. Atopy/allergic background. Immune activation has been anecdotally noted with MCD-like patterns; a few C1q cases occur in that spectrum. (Low-quality evidence.) PMC

9. Genetic susceptibility (theoretical). Variation in complement or immune-regulatory genes may predispose, but this is not well proven. PMC

10. Malignancy-associated immune complexes. Rare adult cases link C1q-dominant GN with cancers, likely via tumor antigen–antibody complexes. Revista Nefrología

11. Chronic antigen exposure. Long-standing exposure to antigens (infections or other sources) can maintain immune-complex formation. PMC

12. Drug-related immune reactions (possible). A few reports suggest medications can trigger immune-complex GN; C1q dominance has been observed rarely. PMC

13. Post-vaccination (rare case reports). Very rare temporal links exist, but causation is unproven. (Low-certainty.) PMC

14. Proliferative GN background. Some C1q cases show a proliferative pattern, hinting that the underlying GN mechanism favors complement deposition. PMC

15. FSGS spectrum overlap. Podocyte injury with secondary immune deposition may produce a C1q-dominant pattern in some FSGS-like cases. PMC

16. Childhood nephrotic syndrome milieu. Higher pediatric biopsy series rates suggest age-related immune responses may favor C1q deposits. PMC

17. Non-lupus hypocomplementemia (uncommon). Although classic C1qN typically lacks lupus-like low complements, exceptions exist with complement changes from other causes. WJNU

18. Bacterial endocarditis/Q-fever (case report level). Infection-associated GN occasionally shows C1q dominance. (Very rare.) ResearchGate

19. Paraneoplastic immune activation. Tumor-driven antibodies can create circulating complexes that deposit in glomeruli with C1q. Revista Nefrología

20. Unknown mixed mechanisms. In many patients, more than one factor—genetic, immune, infectious—likely combines to produce the deposits. PMC

Symptoms and signs

1. Swelling (edema). Puffy eyes in the morning and swelling of feet/ankles by evening are common when protein loss is heavy. PMC

2. Foamy urine. Bubbles or foam suggest proteinuria. PMC

3. Blood in urine. Urine may be tea-colored or microscopic blood is found on testing. PMC

4. Weight gain from fluid. Fluid retention adds weight quickly. PMC

5. High blood pressure. Kidneys help control pressure; disease can raise it. PMC

6. Fatigue and low energy. Loss of protein and fluid shifts make people feel tired. PMC

7. Reduced urine output (in flares). When swollen, urine volume may drop. PMC

8. Abdominal bloating/ascites. Fluid can collect in the belly in severe nephrotic states. PMC

9. Shortness of breath. Fluid overload can cause breathlessness or pleural effusion. PMC

10. Muscle cramps. Mineral shifts and diuretics (if used) can contribute. PMC

11. Loss of appetite or nausea. Uremic symptoms may appear if kidney function worsens. PMC

12. Frequent relapses in children with NS. Kids can cycle through swelling and remission. Turkish Journal of Pediatrics

13. Steroid resistance in some patients. Not everybody improves with steroids. PMC

14. Infections (indirect risk). Heavy protein loss can lower protective proteins, raising infection risk. PMC

15. Clotting risk (indirect risk). Nephrotic syndrome may increase blood clot tendencies. PMC

Diagnostic tests

Physical examination

1. Blood pressure measurement. High readings are common in kidney disease and guide urgency and treatment. PMC

2. Edema check (pitting test). Pressing the shin or ankle leaves a dent if fluid is excess; this tracks severity of swelling day to day. PMC

3. Weight and waist measurement. Rapid changes suggest fluid gain or loss; daily weights help monitor response. PMC

4. Lung and heart exam. Crackles in lungs or fast heart rate may signal fluid overload or hypertension from kidney disease. PMC

5. Skin and joint check for lupus clues. Because C1q nephropathy requires no evidence of SLE, doctors look carefully for rashes, mouth ulcers, or arthritis to rule lupus out. WJNU

Manual bedside tests

6. Urine dipstick at the bedside. A quick strip can detect protein and blood in minutes and helps decide on further tests. PMC

7. Orthostatic edema assessment. Comparing morning-evening swelling patterns helps confirm fluid shifts from protein loss. PMC

8. Jugular venous pressure (JVP) inspection. A raised JVP points to volume overload, guiding diuretics and salt restriction. PMC

9. Bedside albumin/protein review with rapid tests (if available). Point-of-care urine protein:creatinine can be done in some clinics. PMC

10. Dipstick trend logging. Repeated bedside checks over days show whether proteinuria is rising or improving. PMC

Laboratory & pathological tests (the core)

11. Urinalysis with microscopy. Confirms protein, looks for red cells and casts, and screens for infection; it is the first laboratory step. PMC

12. Urine albumin- or protein-to-creatinine ratio (spot) and/or 24-hour protein. These quantify protein loss and define nephrotic-range proteinuria. PMC

13. Serum creatinine and eGFR. Show kidney function at baseline and over time. PMC

14. Serum albumin and lipid profile. Low albumin and high cholesterol support nephrotic syndrome activity. PMC

15. Autoimmune panel to exclude lupus (ANA, anti–dsDNA) and complements (C3/C4). C1q nephropathy is diagnosed only when lupus is not present; complements are often normal. WJNU

16. Infection screen (HBV, HCV, HIV) when appropriate. Helps find secondary causes and guides treatment safely. PMC

17. Kidney biopsy with immunofluorescence, EM, and light microscopy. This is the definitive test: it shows dominant or co-dominant C1q in the mesangium, variable light-microscopy patterns (MCD-like, FSGS, proliferative), and mesangial electron-dense deposits; tubuloreticular inclusions are typically absent. ScienceDirect+2PMC+2

Electrodiagnostic & monitoring tests

18. Electrocardiogram (ECG). Not a kidney test per se, but important if edema, blood-pressure changes, or electrolyte issues develop; it checks rhythm and strain. PMC

19. Ambulatory blood-pressure monitoring (24-hour). Detects masked or nighttime hypertension that can worsen kidney damage. PMC

20. Home blood-pressure and weight logs (digital monitoring). Regular tracking helps spot relapses early and tailor diuretics and diet. PMC

Non-pharmacological treatments (therapies & lifestyle)

1) Daily sodium (salt) restriction
Aim for <2 g sodium/day (<5 g salt). Lower salt helps reduce fluid retention, blood pressure, and protein leak in urine, easing strain on the kidney filters. It also improves the effect of blood-pressure drugs. Read labels, avoid salty snacks and restaurant sauces. Mechanism: less sodium lowers extracellular volume → reduces intraglomerular pressure and proteinuria. OUP Academic+1

2) Moderate protein intake
For most adults with CKD not on dialysis, target ~0.8 g protein/kg/day; avoid very high-protein diets. This level maintains muscle but limits kidney workload and nitrogen waste that can speed CKD. Mechanism: lower filtered amino acid load reduces hyperfiltration stress. KDIGO+1

3) Tight blood-pressure control at home
Use a validated cuff; keep a log. For proteinuric kidney disease, a lower systolic target is often advised when tolerated to slow decline. Mechanism: lower systemic and intraglomerular pressure cuts proteinuria and scarring. (Targets individualized by clinician.) PubMed

4) RAAS-friendly eating (watch high-potassium substitutes)
While fruits/veg are healthy, potassium-based salt substitutes can raise potassium if you’re on ACEi/ARB. Work with a dietitian to balance potassium and phosphorus. Mechanism: prevent hyperkalemia while preserving the benefits of RAAS blockers. KDIGO

5) Weight management
Gradual weight loss if overweight improves blood pressure, metabolic health, and proteinuria. Mechanism: lowers renal hyperfiltration and inflammation linked to adiposity. KDIGO

6) Regular physical activity
Aim for 150 minutes/week of moderate exercise as tolerated. Activity improves BP, insulin sensitivity, lipids, and inflammation—all protective for kidneys. Mechanism: hemodynamic and metabolic improvements reduce glomerular injury. KDIGO

7) Smoking cessation
Stopping tobacco slows CKD progression and cuts cardiovascular risk. Mechanism: reduces endothelial injury and oxidative stress that worsen glomerular damage. KDIGO

8) Nephrotoxin avoidance
Avoid NSAIDs (e.g., ibuprofen), unnecessary contrast dye, and herbal products of unknown safety. Mechanism: prevents afferent arteriolar constriction and direct tubular toxicity that raise creatinine and protein leak. KDIGO

9) Vaccinations (flu, pneumococcal, hepatitis B as indicated)
Immunization lowers severe infection risk, which can trigger kidney relapses or acute kidney injury. Mechanism: reduces inflammatory hits to glomeruli and need for high-dose steroids. KDIGO

10) “Sick-day” plan
When vomiting/diarrhea or fever, follow a clinician-approved plan (pause certain meds, hydrate, check weight/BP). Mechanism: prevents pre-renal AKI and drug accumulation. KDIGO

11) Edema self-care
Daily weights, leg elevation, and compression stockings (if appropriate) help swelling along with salt control. Mechanism: lowers venous pressure and interstitial fluid. KDIGO

12) Sleep and possible OSA evaluation
Treating sleep apnea improves BP and inflammation. Mechanism: stabilizes nocturnal sympathetic tone and renin–angiotensin activation that harm kidneys. KDIGO

13) Stress-reduction practice
Brief daily mindfulness or relaxation may reduce BP and stress hormones that injure glomeruli over time. Mechanism: autonomic balance → lower hemodynamic stress. KDIGO

14) Individualized fluid guidance
In edema, modest fluid moderation may help; in euvolemia, avoid unnecessary restriction. Mechanism: volume balance prevents hypo/hypervolemic kidney hits. KDIGO

15) Diabetes risk and glucose care
If you have diabetes or prediabetes, keep A1c individualized; SGLT2 inhibitors and diet/activity help the kidney, even without diabetes in CKD. Mechanism: lowers intraglomerular pressure and tubular stress. New England Journal of Medicine+1

16) Lipid management & heart-healthy diet
Use dietary patterns rich in vegetables, whole grains, and unsalted beans; limit refined sugar and trans-fat. Mechanism: improves endothelial health and lowers CKD cardiovascular risk. KDIGO

17) Home urine checks when advised
Periodic dipstick or lab urine protein/creatinine checks help catch relapses early. Mechanism: earlier therapy adjustments reduce scarring. KDIGO

18) Medication adherence & pill review
Bring all medicines/supplements to visits; check for interactions that raise potassium or harm kidneys. Mechanism: safer regimens and consistent RAAS/SGLT2 benefit. KDIGO

19) Pregnancy planning & contraception (if relevant)
Discuss safe timing and drugs before conception; some immunosuppressants are teratogenic. Mechanism: reduces fetal risk and disease flare. PubMed

20) Patient education & support
Understand your targets (BP, sodium, protein intake, albuminuria), warning signs, and follow-up schedule. Mechanism: informed self-care improves long-term kidney outcomes. KDIGO

Drug treatments

Important: No drug is FDA-approved specifically for “C1q nephropathy.” Therapies are extrapolated from proteinuric glomerular disease and case reports. Doses below are common ranges—your nephrologist will tailor them.

1) Prednisone (oral glucocorticoid)
Used first in many with nephrotic syndrome features; may induce remission when disease behaves like minimal-change. Mechanism: broad anti-inflammatory and immunosuppressive effects on podocytes and immune cells. Typical adult starting doses vary (e.g., 0.5–1 mg/kg/day short term, then taper). Main risks: infection, hyperglycemia, bone loss. (FDA label anchor: prednisone class safety.) FDAaccessdata

2) Methylprednisolone (IV pulses in severe relapse)
Given as short IV pulses for marked edema or heavy proteinuria, then switch to oral taper. Mechanism: rapid immune dampening and podocyte stabilization. Risks include glucose spikes and infection. (Label anchor for systemic steroid safety.) FDAaccessdata

3) Tacrolimus (calcineurin inhibitor)
Useful for steroid-resistant or steroid-dependent cases; several C1qN series report remission with tacrolimus. Typical trough-guided dosing per transplant labels; in GN, lower targets are often used by specialists. Mechanism: blocks T-cell activation; stabilizes podocyte actin cytoskeleton. Key risks: nephrotoxicity, hypertension, diabetes. PMC+2FDAaccessdata+2

4) Cyclosporine (calcineurin inhibitor)
Alternative to tacrolimus when steroids fail or cause side effects. Mechanism and risks similar to tacrolimus; dose is trough-guided. Case series suggest remission in steroid-resistant nephrotic syndrome with C1qN. PMC+1

5) Mycophenolate mofetil (MMF)
Often used as a steroid-sparing agent; lowers lymphocyte proliferation (IMPDH inhibition). Adult dosing commonly 1–2 g/day split, individualized for tolerance. Risks: GI upset, leukopenia, teratogenicity; monitor CBC. (Label anchor.) FDAaccessdata+1

6) Rituximab (anti-CD20 monoclonal antibody)
Considered for frequent relapses or CNI intolerance; case reports/series show remissions in C1qN. Common GN regimens: 375 mg/m² weekly ×4 or 1 g ×2 two weeks apart (per specialist protocol). Risks: infusion reactions, PML, HBV reactivation; screen HBV. (FDA label anchor.) PMC+2OUP Academic+2

7) Cyclophosphamide
Selected refractory cases, especially with aggressive histology, may receive limited courses plus steroids. Mechanism: alkylating immunosuppression. Dosing is individualized (e.g., monthly IV pulses or oral low dose); watch fertility, cytopenias, bladder toxicity. (Label anchor.) FDAaccessdata+1

8) Azathioprine
Sometimes used for maintenance when other agents are not tolerated. Mechanism: purine antimetabolite lowering lymphocyte proliferation. Need TPMT/NUDT15 consideration; monitor CBC/LFTs. (Label anchor: malignancy warning.) FDAaccessdata

9) ACE inhibitor (e.g., lisinopril)
Foundation therapy for proteinuria and kidney protection, with dose titrated to BP and potassium. Mechanism: lowers intraglomerular pressure and protein leak by RAAS blockade. Risks: cough, hyperkalemia, rise in creatinine after start—monitor labs. (Label anchor.) FDAaccessdata

10) ARB (e.g., losartan)
Use if ACEi not tolerated, or combine cautiously only under specialist oversight. Mechanism and benefits similar to ACEi for proteinuria reduction. Monitor potassium and kidney function. (Label anchor.) FDAaccessdata+1

11) SGLT2 inhibitor (dapagliflozin)
For CKD at risk of progression—with or without diabetes—dapagliflozin 10 mg daily reduces eGFR decline and ESKD, on top of ACEi/ARB, when appropriate. Mechanism: restores tubuloglomerular feedback → lowers intraglomerular pressure. Watch for mycotic infections; hold during acute illness. (FDA CKD label; DAPA-CKD trial.) FDAaccessdata+1

12) Loop diuretic (e.g., furosemide)
Relieves edema; dose individualized to urine response. Mechanism: inhibits NKCC2 in loop of Henle to promote sodium/water excretion. Monitor electrolytes and kidney function; avoid dehydration. (Label anchor.) FDAaccessdata

13) Vitamin D analogs (e.g., calcitriol when indicated)
In CKD with secondary hyperparathyroidism, active vitamin D can help bone/mineral balance and may modestly lower proteinuria in some settings; dosing individualized to calcium/phosphate. Mechanism: VDR-mediated anti-proteinuric and anti-inflammatory effects. (Label anchors + clinical data context.) FDAaccessdata+1

14) Statins (e.g., atorvastatin)
Manage dyslipidemia common in nephrotic states to lower CV risk. Mechanism: HMG-CoA reductase inhibition reduces LDL and inflammation. (Use per lipid guidelines; label-anchored for safety/indications.) KDIGO

15) Pneumocystis prophylaxis (TMP-SMX) when on heavy immunosuppression
Your team may add low-dose TMP-SMX if you receive high-dose steroids or multi-agent immunosuppression. Mechanism: prevents opportunistic infection that can trigger AKI. (Label-anchored safety and use; individualized.) KDIGO

16) Gastric protection when on steroids
A PPI or H2 blocker may be used short-term to prevent GI bleeding in high-risk patients on glucocorticoids. Mechanism: reduces acid injury. (Use case-by-case per guidelines.) KDIGO

17) Blood-pressure medicines beyond RAAS blockers
Dihydropyridine calcium-channel blockers or beta-blockers may be added to hit targets if needed. Mechanism: BP lowering slows kidney damage. (Guideline context.) PubMed

18) Erythropoiesis-stimulating agent (if anemic from CKD)
Used when anemia is due to CKD and iron is corrected. Mechanism: raises red blood cell production; targets are individualized. (Guideline context.) KDIGO

19) Rituximab retreatment (selected relapsers)
If you responded to rituximab but relapsed, specialists may repeat dosing using established GN schedules. Mechanism: re-depletes pathogenic B cells. Monitor for infections and HBV. (Label anchor; case data). FDAaccessdata+1

20) Transition plans (tapering & maintenance)
After remission, clinicians taper steroids and choose a low-toxicity maintenance agent (e.g., MMF) or watchful monitoring to limit cumulative side effects. Mechanism: balances relapse prevention and safety. (Guideline approach to GN care). PubMed

Dietary molecular supplements

1) Omega-3 fatty acids (EPA/DHA)
Some studies suggest omega-3s can lower proteinuria or slow kidney events, while others show neutral albuminuria effects but better triglycerides and arterial stiffness. Typical used doses: ~2–4 g/day combined EPA+DHA with meals. Mechanisms include anti-inflammatory lipid mediators and BP improvement. PMC+1

2) Curcumin (turmeric extracts)
Meta-analyses and small trials suggest curcumin may reduce proteinuria; others show no tubular biomarker benefit. Practical doses in studies vary (e.g., 500–1500 mg/day standardized extract). Mechanisms: antioxidant and NF-κB/Nrf2 modulation. PubMed+1

3) Nutritional vitamin D3 (cholecalciferol) when deficient
Correcting deficiency supports bone health and may modestly lower proteinuria in some CKD cohorts; dose per 25-OH-D level (e.g., 1000–4000 IU/day). Mechanism: immune and podocyte effects via VDR signaling. JAMA Network+1

4) Coenzyme Q10
Small studies in CKD suggest possible BP and endothelial benefits; typical doses 100–300 mg/day with fat-containing meals. Mechanism: mitochondrial antioxidant improving endothelial function. Evidence remains limited. Clinical Nutrition Journal

5) Probiotics
Investigated to reduce gut-derived uremic toxins; strains and doses vary. Possible small improvements in inflammation; discuss if immunosuppressed. Mechanism: alters gut microbiome to reduce toxin generation. KDIGO

6) Resveratrol
Preclinical and small human data suggest anti-inflammatory and antioxidant effects; dosing varies (100–500 mg/day in studies). Use cautiously with anticoagulants. KDIGO

7) N-acetylcysteine (NAC)
Antioxidant with potential endothelial benefits; typical oral doses 600–1200 mg/day in divided doses. Evidence in CKD is mixed. KDIGO

8) Magnesium (if low and approved)
Correct documented deficiency to support BP and endothelial function; avoid excess with advanced CKD. Dose individualized. KDIGO

9) Plant polyphenols (e.g., green tea catechins)
Potential anti-inflammatory and anti-fibrotic actions; watch caffeine content and liver safety with concentrated extracts. Dosing varies. KDIGO

10) Fiber supplements (psyllium/inulin)
May modestly improve cardiometabolic markers and bind uremic toxin precursors; titrate to tolerance. Mechanism: microbiome and lipid effects. KDIGO

Immunity-booster / regenerative / stem-cell drugs

A) There is no FDA-approved “immunity-booster” or stem-cell drug for C1q nephropathy. Current care uses immunosuppressants listed above. Experimental regenerative options (e.g., mesenchymal stem cells or their extracellular vesicles) are under study for CKD and some glomerular diseases; early trials suggest safety signals and potential benefit, but these are not standard care. If you see such offers, treat them as research only and discuss with your nephrologist. BioMed Central+1

1) Mesenchymal stem cells (MSC) — experimental
Mechanism: paracrine anti-inflammatory, antifibrotic effects; possible microvascular support. Dosing and routes vary in trials; not approved for CKD/C1qN. PMC

2) MSC-derived extracellular vesicles — experimental
Early CKD work suggests safety and anti-inflammatory effects; not approved; only in clinical studies. Frontiers

3) Low-dose rituximab “immune reset” (off-label, specialist)
In C1qN case reports, lower rituximab dosing achieved remission; still immunosuppressive, not an “immune booster.” Dosing individualized. PMC

4) Vitamin D receptor activation (calcitriol) for immune modulation (adjunct)
Used for CKD-MBD; may have modest immunomodulatory benefits but is not a regenerative drug. Dose based on labs. AJKD

5) SGLT2 inhibitor (dapagliflozin) “kidney-protective” (adjunct)
Not an immune booster; reduces CKD progression across etiologies via hemodynamic and tubular mechanisms. Standard 10 mg daily if eligible. FDAaccessdata

6) Lifestyle “immune resilience” bundle (sleep, vaccines, nutrition)
Practical, proven risk-reduction strategies that limit infection triggers and inflammatory hits. Not a drug, but essential. KDIGO

Procedures / Surgeries

1) Kidney biopsy (diagnostic)
Needed to confirm C1q-dominant deposits and exclude other causes; guides therapy. Needle biopsy under imaging. Why: only pathology can diagnose C1qN with confidence. AJKD

2) Tunneled dialysis catheter (when urgent dialysis is needed)
Placed in a central vein to start hemodialysis quickly in severe kidney failure. Why: emergency access for life-saving dialysis. KDIGO

3) Arteriovenous fistula creation
Surgical connection of artery to vein in the arm for long-term hemodialysis. Why: the safest durable access once dialysis is needed. KDIGO

4) Peritoneal dialysis catheter placement
Soft tube into the abdomen for home peritoneal dialysis. Why: offers home-based dialysis when kidneys fail. KDIGO

5) Kidney transplantation
For end-stage disease; offers best quality-of-life and survival for suitable patients. Why: replaces failed kidney; requires lifelong immunosuppression. KDIGO

Preventions

1. Keep sodium <2 g/day and meet your BP goal. Mechanism: reduces intraglomerular pressure. OUP Academic

2. Take ACEi/ARB (and SGLT2i if eligible) as prescribed. Mechanism: proven kidney protection in CKD. FDAaccessdata

3. Maintain healthy weight and exercise regularly. Mechanism: lowers hyperfiltration and inflammation. KDIGO

4. Avoid NSAIDs and unnecessary contrast dyes. Mechanism: prevents AKI hits. KDIGO

5. Get influenza, pneumococcal, and HBV vaccines if indicated. Mechanism: fewer infections and relapses. KDIGO

6. Monitor urine protein and kidney labs on schedule. Mechanism: early detection of relapse. KDIGO

7. Treat sleep apnea if present. Mechanism: BP and sympathetic tone improve. KDIGO

8. Stop smoking. Mechanism: reduces endothelial injury. KDIGO

9. Plan pregnancy with your nephrologist. Mechanism: avoids teratogens and flare risk. PubMed

10. Keep a “sick-day” plan to avoid dehydration and AKI. Mechanism: prevents preventable kidney hits. KDIGO

When to see a doctor urgently

See your doctor (or urgent care/ER) if you have fast swelling of legs/face, sudden weight gain >1–2 kg in days, very high blood pressure, shortness of breath, severe decrease in urine, visible blood in urine, fever or cough while on immunosuppressants, severe abdominal pain, confusion, or if you are pregnant or planning pregnancy. These can signal relapse, clot, infection, or acute kidney injury that needs quick treatment. PubMed

Foods to favor & to limit/avoid

Eat more:

1. Fresh fruits/vegetables within potassium guidance;

2. Whole grains;

3. Unsalted beans/lentils as protein budget allows;

4. Fish (omega-3 rich);

5. Olive/canola oil;

6. Yogurt or fortified alternatives (phosphorus/potassium checked);

7. Egg whites;

8. Oats/barley;

9. Nuts in small portions (watch potassium/phosphorus);

10. High-fiber foods (psyllium as advised). Mechanisms: cardiometabolic benefits and BP/proteinuria support. KDIGO

Limit/avoid:

1. Salty packaged snacks;

2. Restaurant/fast foods;

3. Processed meats;

4. Instant noodles/soups;

5. High-sodium sauces (soy, ketchup);

6. Energy drinks;

7. Excess red meat/high-protein fads;

8. Potassium salt substitutes if on ACEi/ARB;

9. Phosphate-additive colas;

10. Herbal remedies with unknown kidney safety. Mechanisms: reduce sodium load, hidden phosphorus/potassium, and nephrotoxins. OUP Academic+1

Frequently asked questions

1) Is C1q nephropathy an autoimmune disease?
It is a pattern of immune deposits rather than one autoimmune illness; many cases behave like minimal-change disease or FSGS. Treatment follows proteinuric GN principles. AJKD

2) Can it go into remission?
Yes, many patients achieve partial or complete remission with steroids, CNIs, or rituximab; evidence comes from case series and reports. PMC+1

3) Which blood-pressure drugs protect the kidney most?
ACE inhibitors or ARBs reduce proteinuria and slow CKD; they are core therapy if tolerated. FDAaccessdata+1

4) Do SGLT2 inhibitors help even without diabetes?
Yes—dapagliflozin reduced CKD progression across diabetic and non-diabetic CKD in DAPA-CKD and is FDA-labeled for CKD risk reduction. New England Journal of Medicine+1

5) Are there drugs approved specifically for C1qN?
No. Therapies are off-label, guided by kidney-disease guidelines and small C1qN series. PubMed

6) Will I need a biopsy?
Usually yes. Diagnosis requires seeing dominant C1q deposits by immunofluorescence. AJKD

7) What is the steroid plan?
Often a limited course to induce remission, then taper to minimize side effects; exact regimen is individualized. FDAaccessdata

8) What if I’m steroid-resistant?
Doctors may use tacrolimus or cyclosporine; if relapsing/intolerant, rituximab or MMF can be considered. PMC+2FDAaccessdata+2

9) Are stem-cell treatments available now?
Only in research. No approved stem-cell therapy for C1qN; discuss clinical trials cautiously. BioMed Central

10) Can diet alone cure it?
Diet cannot cure C1qN, but low sodium, adequate protein control, and healthy weight meaningfully support medical therapy. OUP Academic+1

11) How often should labs be checked?
Early on, usually every 2–4 weeks to track creatinine, potassium, and urine protein, then less often in stable phases, per your clinician. KDIGO

12) Are vaccines safe on immunosuppression?
Inactivated vaccines are recommended; avoid live vaccines on strong immunosuppression. Coordinate timing with your team. KDIGO

13) What are key drug side effects to watch?
CNIs can raise creatinine and BP; steroids increase infection, glucose, and bone loss; rituximab can cause infusion reactions and HBV reactivation. Report fevers promptly. FDAaccessdata+2FDAaccessdata+2

14) Will I always leak protein?
Some reach complete remission; others have partial reduction. Early and consistent care increases the odds of better control. PMC

15) What’s the long-term outlook?
Variable. With BP control, RAAS blockade/SGLT2i when appropriate, and individualized immunotherapy, many stabilize; a minority progress to advanced CKD. Close follow-up matters. KDIGO

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: November 07, 2025.

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C1q Deficiency

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CADDS

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