W. G. M. Rivero, MD ← All Guides
HIV · Kidney Disease · Patient Guide

HIVAN: The Kidney Disease You Can Fight Back Against

HIV can harm your kidneys — but starting treatment changes everything

HIV-associated nephropathy (HIVAN) is a serious but treatable kidney disease that develops in people living with HIV whose virus is not well controlled. The good news: starting or optimizing your HIV medications can stop — and even reverse — the damage. This guide explains what HIVAN is, what to watch for, and how to protect your kidneys for life.

Author: W. G. M. Rivero, MD, FPCP, DPSN Specialty: Internal Medicine · Nephrology Last Reviewed:
Section 1

What Is HIVAN?

HIV and the Kidneys

HIV does not just affect your immune system. The virus can directly infect cells in your kidneys — particularly the filtering cells called podocytes — causing them to collapse and scar. This is called HIV-associated nephropathy, or HIVAN. It is one of the most serious kidney complications of HIV, but it is also one of the most responsive to treatment when caught early.

Who Is at Higher Risk?

HIVAN is most common in people whose HIV is not under control — those with a high viral load and low CD4 count. It is more common in people of African ancestry due to a gene called APOL1. In the Philippines, HIVAN is increasingly seen in MSM (men who have sex with men) and individuals presenting late to HIV care. People who have stopped or never started HIV treatment are at highest risk.

HIVAN is not the same as kidney damage from HIV medications

Some older HIV drugs — particularly tenofovir DF (TDF), found in older regimens — can also harm the kidneys, but through a different mechanism. Both are preventable and manageable with the right treatment. Your doctor can tell which type of kidney problem you have and adjust your medications accordingly.

Section 2

Symptoms and Warning Signs

⚠

HIVAN is often silent in the early stages

Many patients feel completely normal while significant kidney damage is already occurring. Do not wait for symptoms — if you are living with HIV, regular kidney monitoring is essential.

Early signs (often missed)

Foamy or frothy urine (protein leaking into urine); slightly elevated blood pressure; mild swelling of the ankles by end of day; fatigue that seems worse than usual.

Later signs (seek care immediately)

Marked swelling of legs, feet, and face; very foamy urine that persists; high blood pressure that is difficult to control; decreased urine output; severe fatigue, loss of appetite, and nausea.

Foamy urine is one of the most important warning signs — it means protein is leaking through damaged kidney filters. Hold a glass of your urine up to the light. If it looks like beer foam that persists for more than a minute, tell your doctor immediately.

Section 3

How Is It Diagnosed?

1

Blood test (creatinine and eGFR)

This measures how well your kidneys filter waste. Your doctor calculates your eGFR — a number that tells you what percentage of kidney function you have left. Normal is above 60.

2

Urine test (protein)

A urine dipstick or urine protein-creatinine ratio (UPCR) checks how much protein is leaking. HIVAN typically causes heavy protein leakage — often more than 3.5 grams per day (called nephrotic-range proteinuria).

3

Kidney ultrasound

In HIVAN, kidneys are often enlarged and echogenic (appear bright on ultrasound) — the opposite of most other kidney diseases where kidneys shrink. This is an important clue for your doctor.

4

Kidney biopsy (sometimes needed)

A small needle sample of kidney tissue is examined under a microscope. The pattern seen in HIVAN is called "collapsing FSGS" — scarred, collapsed kidney filters. Not everyone needs a biopsy; your doctor will decide based on your situation.

5

HIV viral load and CD4 count

These confirm HIV status and degree of immune suppression. HIVAN is most common when viral load is high and CD4 is low.

Section 4

Treatment

●

The most powerful treatment for HIVAN is HIV medication (ART)

Starting or optimizing your HIV treatment can stop kidney damage — and in many patients, kidney function actually improves after viral suppression is achieved.

1

Start or optimize your HIV medications (ART)

If you are not yet on HIV treatment, start immediately — do not wait. If you are already on treatment but your viral load is detectable, speak to your HIV doctor about adjusting your regimen. The goal is undetectable viral load (HIV RNA <50 copies/mL).

2

Use the right HIV medications

Some HIV drugs are safer for kidneys than others. Tenofovir alafenamide (TAF — found in newer combinations like Biktarvy or Descovy) is much safer for kidneys than the older tenofovir DF (TDF — in older pills like Truvada or Atripla). Tell your doctor if you are still on TDF so you can discuss switching.

3

Blood pressure control with an ACE inhibitor or ARB

These blood pressure medications do double duty — they lower blood pressure AND reduce protein leakage from damaged kidneys. Common examples: enalapril, lisinopril (ACE inhibitors) or losartan, valsartan (ARBs). Take them every day, even when you feel well.

4

Avoid kidney-harmful medications

NSAIDs (ibuprofen, mefenamic acid, aspirin for pain) damage kidneys — use paracetamol instead. Herbal and traditional remedies — many are toxic to kidneys; tell your doctor about everything you take. If you need a CT scan with contrast dye, make sure your doctor knows about your kidney disease beforehand.

Section 5

Protecting Your Kidneys Long-Term

Stay on your HIV medications — every day

Missing doses allows the virus to replicate and re-damage kidney cells. Even brief treatment interruptions can cause significant setbacks. If you are having trouble taking medications — due to cost, side effects, or stigma — tell your HIV care team. There are assistance programs and solutions available.

Get your kidneys checked regularly

Your doctor should check your creatinine, eGFR, and urine protein at every visit — or at minimum every 6 months. More frequent monitoring (every 3 months) is recommended if you are on TDF, have diabetes or hypertension, or already have reduced kidney function.

Control blood pressure

Target: below 130/80 mmHg with HIVAN. Take your ACE inhibitor or ARB every day. Reduce salt intake. Maintain a healthy weight. Blood pressure control is one of the most important things you can do to slow kidney disease progression.

Protect what remains — avoid all nephrotoxins

No NSAIDs for pain — use paracetamol. No traditional herbal medicines without disclosing them to your doctor. Drink adequate water (6–8 glasses per day unless your doctor restricts fluids). Avoid heavy alcohol — it raises blood pressure and worsens kidney disease.

Nutrition

Adequate protein intake is generally appropriate in early HIVAN — speak to a dietitian, as restriction is not always needed. Reduce salt to control blood pressure and swelling. Control blood sugar if you have diabetes.

Section 6

Living With Kidney Disease and HIV

If your kidneys fail

Kidney failure from HIVAN is not a death sentence. Both hemodialysis (HD) and peritoneal dialysis (PD) are available for people living with HIV and work just as well as in HIV-negative patients. HIV is no longer a barrier to kidney transplant — in the Philippines, HIV-positive patients can be evaluated for transplant if HIV is well controlled on ART.

Mental health and adherence

Living with both HIV and kidney disease is a significant burden. Depression and stigma are real barriers to medication adherence. Speak openly with your care team. Support groups for PLHIV exist in major Philippine cities. Poor mental health directly affects ART adherence, which directly affects kidney outcomes — treating both together matters.

Your care team

Managing HIVAN requires coordination between your HIV specialist (infectious disease or internal medicine), your nephrologist, and your primary care physician. Bring a complete medication list to every visit. Ask for a written care plan if your appointments are with different doctors on different days.

Section 7

Common Questions

Can HIVAN be reversed?

Yes — in many patients, especially when HIVAN is caught early and ART is started promptly, kidney function stabilizes and protein in the urine decreases significantly. Some patients recover kidney function they had already lost. The key is starting treatment quickly.

Do I need a kidney biopsy?

Not always. If you have HIV, heavy protein in your urine, and enlarged kidneys on ultrasound, your doctor may treat you for HIVAN without a biopsy. A biopsy is recommended when the diagnosis is uncertain, when other kidney diseases need to be ruled out, or when the kidneys are worsening despite ART.

Can I still get a kidney transplant if I have HIV?

Yes. HIV-positive kidney transplant is now performed in specialized centers. PLHIV with well-controlled HIV (undetectable viral load) on stable ART are eligible for evaluation. Outcomes are comparable to HIV-negative recipients. Discuss this with your nephrologist if you are approaching kidney failure.

Is HIVAN contagious — can my family members get kidney disease from me?

No. HIVAN is not transmitted to others. Only HIV itself is transmitted (through blood, sexual contact, or mother-to-child). Your kidney disease is a complication of your own HIV infection — it cannot spread to anyone else.

I stopped my HIV medications two years ago. Now my kidneys are damaged — will they recover if I restart?

Possibly, especially if you restart early. The earlier you restart ART after stopping, the better the chance of kidney recovery. Some damage may be permanent if HIVAN has been active for a long time. Restart ART immediately and work with your nephrologist to assess how much function can be recovered.

My doctor wants me on a blood pressure pill even though my blood pressure seems normal — why?

ACE inhibitors and ARBs are prescribed in HIVAN not just for blood pressure but to reduce protein leakage from damaged kidneys, which slows progression even in patients with normal blood pressure. Take them as prescribed.

Dr. W. G. M. Rivero

W. G. M. Rivero, MD, FPCP, DPSN

This guide was written to help patients living with HIV understand their kidney health — and take control of it. HIVAN is one of the few kidney diseases where starting the right treatment can genuinely reverse damage. You have more power here than you may realize.

Internal Medicine · Nephrology · Philippines · williamriveromd.com

Medical Disclaimer: This guide is for patient education purposes only and does not constitute personalized medical advice. Treatment decisions for HIVAN, HIV medications, and kidney disease management must be made in partnership with your HIV specialist and nephrologist. Medication protocols referenced here reflect current Philippine and international guidelines and may change over time.
⚕ Clinician Reference KDIGO 2024 🇵🇭 Philippines Context

HIVAN: The Kidney Disease You Can Fight Back Against

Pathophysiology, diagnostic algorithm, ART-based treatment, and CKD management in PLHIV

Practical clinical guide to HIV-associated nephropathy (HIVAN) and the broader spectrum of HIV-related kidney disease — covering pathophysiology, diagnostic workup including biopsy interpretation, ART optimization, proteinuria management, CKD progression, and ESKD management in PLHIV. Philippine epidemiologic context included.

Author: W. G. M. Rivero, MD, FPCP, DPSN Specialty: Internal Medicine · Nephrology Last Reviewed:
Section 1

HIV-Related Kidney Disease Spectrum

Entity Mechanism Biopsy Pattern Key Clinical Feature Treatment Focus
HIVAN Direct HIV podocyte infection + APOL1 susceptibility Collapsing FSGS + microcystic tubular dilatation Nephrotic proteinuria; enlarged echogenic kidneys; rapid progression ART + ACEi/ARB; corticosteroids for select cases
HIVICK (HIV Immune Complex Kidney Disease) Immune complex deposition IgA nephropathy-like; membranous nephropathy; MPGN; lupus-like (FHLS) Subnephrotic proteinuria + hematuria; may occur at any CD4 count ART + immunosuppression for select cases
TDF nephrotoxicity Mitochondrial toxicity in proximal tubules Proximal tubular injury; may show features of Fanconi syndrome Normoglycemic glucosuria, hypophosphatemia, tubular proteinuria (β2-MG elevated) Stop TDF; switch to TAF; electrolyte replacement
Thrombotic microangiopathy (TMA) HIV-related endothelial injury; drug-induced (e.g., indinavir) TMA pattern Microangiopathic hemolytic anemia + thrombocytopenia + AKI ART optimization; plasma exchange if severe
Comorbidity-driven CKD Hypertension, diabetes, aging HTN nephrosclerosis; diabetic nephropathy Gradual progression; less proteinuric than HIVAN Risk factor control
⚠

Philippines context

In the Philippines, HIVAN is increasingly reported in MSM presenting late to HIV care with advanced immunosuppression. HIV testing should be offered to all patients with unexplained nephrotic-range proteinuria, especially young males with rapid CKD progression and enlarged echogenic kidneys on ultrasound.

Section 2

Pathophysiology

1

Direct podocyte infection

HIV-1 infects podocytes and tubular epithelial cells via CD4-independent mechanisms (galactosylceramide receptor). Infected podocytes undergo dedifferentiation, proliferation, and collapse — the hallmark of collapsing FSGS. This is distinct from secondary FSGS where podocytes are injured but not directly infected.

2

APOL1 susceptibility

APOL1 G1 and G2 risk alleles dramatically amplify HIVAN risk (OR >29 for two-allele carriers). These variants are predominantly found in individuals of sub-Saharan African ancestry. In the Philippine context, mixed ancestry patients with African heritage may carry risk alleles — genotyping is available in research settings but not routine clinical practice.

3

Microcystic tubular dilatation

In addition to glomerular collapse, tubular cells undergo cystic dilatation — a feature that is nearly pathognomonic for HIVAN on biopsy and helps distinguish it from other collapsing glomerulopathies (e.g., interferon-associated, pamidronate-associated).

4

Viral suppression reverses the lesion

Because HIVAN is driven by active viral replication in renal cells, achieving undetectable HIV RNA with ART removes the primary driver of injury. Biopsy-proven HIVAN can show partial or complete histologic resolution after sustained viral suppression — a unique feature not seen in primary FSGS.

Section 3

Clinical Presentation

Feature HIVAN Primary FSGS Diabetic Nephropathy
Proteinuria Nephrotic range (>3.5 g/day); often massive Variable; typically nephrotic Microalbuminuria → nephrotic range over years
Progression rate Weeks to months without ART Months to years Years to decades
Kidney size (ultrasound) Enlarged, echogenic Normal or reduced Normal early; reduced late
Hematuria Absent or minimal Absent Absent
Hypoalbuminemia / edema Common; often severe Common Variable
CD4 count at diagnosis Typically <200 cells/μL (classic) N/A N/A
Viral load Usually detectable N/A N/A
Response to ART Dramatic — hallmark feature Not applicable Not applicable
Section 4

Diagnostic Workup

1

Urine studies

Urine dipstick (protein 3+ or 4+ typical); spot urine protein-creatinine ratio (UPCR >3 g/g in nephrotic HIVAN); urine β2-microglobulin or RBP if TDF nephrotoxicity is suspected alongside HIVAN; urine microscopy (oval fat bodies, fatty casts in nephrotic syndrome; no active sediment in isolated HIVAN).

2

Serum studies

Creatinine + eGFR (CKD-EPI); albumin (hypoalbuminemia in nephrotic syndrome); electrolytes including phosphate (hypophosphatemia suggests TDF Fanconi syndrome); HIV RNA viral load + CD4 count; lipid panel (nephrotic dyslipidemia); HBsAg, anti-HCV (co-infections affect kidney disease risk and management); glucose (diabetes screen).

3

Kidney ultrasound

Enlarged, echogenic kidneys are nearly diagnostic in the right clinical context (young PLHIV, high viral load, nephrotic proteinuria). Absence of hydronephrosis excludes obstructive cause. Normal or small kidneys should prompt consideration of non-HIVAN diagnoses.

4

Kidney biopsy — when to perform

Biopsy is recommended when: (a) diagnosis is uncertain; (b) subnephrotic proteinuria makes HIVICK a consideration; (c) kidneys are not enlarged; (d) patient is on TDF and both HIVAN and TDF nephrotoxicity need to be distinguished; (e) ART-naive with rapid deterioration requiring urgent diagnosis. Light microscopy: collapsing FSGS + microcystic tubular dilatation. Immunofluorescence: typically negative (no immune deposits — distinguishes from HIVICK). Electron microscopy: tubuloreticular inclusions in endothelial cells (interferon effect — seen in HIVAN and HIVICK).

5

Differential diagnosis algorithm

Enlarged kidneys + nephrotic proteinuria + detectable HIV + CD4 <200 → empiric HIVAN diagnosis acceptable; start ART. Normal/small kidneys + nephrotic proteinuria + HIV → biopsy required. Subnephrotic proteinuria + hematuria + HIV → HIVICK more likely → biopsy. Tubular proteinuria + glucosuria + hypophosphatemia + HIV on TDF → TDF Fanconi syndrome → stop TDF, switch to TAF.

Section 5

Treatment

ART — First-Line Nephroprotection

Intervention Protocol Evidence Notes
ART initiation/optimization Start immediately regardless of CD4 count; achieve undetectable viral load Level A (INSIGHT START; multiple HIVAN cohort studies) Do not delay ART for biopsy. Viral suppression is more important than diagnostic certainty in rapidly progressive HIVAN.
INSTI-based preferred regimen DTG + TAF/FTC (Descovy) or BIC/TAF/FTC (Biktarvy) Expert consensus Avoid TDF in CKD G3+. DTG does not require renal dose adjustment. Avoid cobicistat-boosted regimens in CrCl <30.
Switch TDF → TAF All PLHIV with CrCl <50 or HIVAN diagnosis DISCOVER trial; HIVAN observational data TAF reduces plasma tenofovir exposure by 90% — dramatically less proximal tubular toxicity.
ACEi or ARB Enalapril 5–20 mg/day, lisinopril 5–20 mg/day, or losartan 25–100 mg/day; titrate to BP <130/80 and maximum tolerated proteinuria reduction Level B (observational + small RCTs) Combination ACEi + ARB increases AKI and hyperkalemia risk — avoid dual RAAS blockade. Monitor K&sup+ and creatinine at 2 and 4 weeks after initiation.
Corticosteroids Prednisone 1 mg/kg/day × 2–4 weeks, taper over 2–3 months Level C (case series; conflicting RCT data) Reserved for rapidly progressive HIVAN not responding to ART within 4–8 weeks, or biopsy showing active inflammation. Weigh infection risk — PLHIV on high-dose steroids require PCP prophylaxis (TMP-SMX DS 3×/week) and careful monitoring.

Monitoring After ART Initiation

●

Expected treatment response

Expect proteinuria to decrease and eGFR to stabilize within 4–12 weeks of viral suppression. If no improvement within 3 months of undetectable viral load — reconsider diagnosis, add ACEi/ARB if not yet started, or consider corticosteroids.

Section 6

HIVICK and Other HIV Immune Complex Diseases

Entity Biopsy Pattern IF/EM Findings Clinical Clue Management
IgA nephropathy-like HIVICK Mesangial hypercellularity IgA + C3 mesangial deposits Subnephrotic proteinuria + microscopic hematuria; may occur at any CD4 ART; ACEi/ARB; immunosuppression for rapid progression
Membranous nephropathy-like Subepithelial deposits IgG + C3 subepithelial Heavy proteinuria; exclude PLA2R-associated primary MN ART; immunosuppression per clinical severity
MPGN pattern Lobular glomerulonephritis IgG, IgM, C3 mesangial + subendothelial Often with HCV co-infection Treat HCV first; ART; consider immunosuppression
Lupus-like HIVICK (FHLS) Diffuse proliferative + capillary wall deposits Full-house (IgG, IgM, IgA, C3, C1q) Mimics lupus nephritis; ANA may be low-titer Rule out true SLE; ART; consider hydroxychloroquine ± immunosuppression
⚠

HIVICK vs. HIVAN

HIVICK can occur at any CD4 count and viral load level — unlike classic HIVAN which requires active viral replication. Biopsy is essential for diagnosis. Treatment approach differs significantly from HIVAN.

Section 7

ESKD Management in PLHIV

Hemodialysis

Both HD and PD are viable in PLHIV. HIV is not a contraindication to dialysis. Outcomes in PLHIV on ART are approaching those of HIV-negative ESKD patients. Universal precautions apply — HIV-positive HD patients do not require dedicated machines or separate shifts in centers with proper infection control. ART is continued through dialysis (see Module 14 for dose adjustments by CrCl stage).

Peritoneal Dialysis

PD is acceptable and may offer advantages including home-based treatment and longer preservation of residual renal function. PD peritonitis rates in HIV-positive patients on ART are comparable to HIV-negative patients. IP antibiotic protocols are the same as for HIV-negative patients (see Module 12 for peritonitis management).

Kidney Transplant

HIV is no longer an absolute contraindication to kidney transplantation. Eligibility criteria: undetectable viral load on stable ART, CD4 >200 cells/μL (some centers accept lower with caution), no active opportunistic infections, no active malignancy. HIV D+/R+ transplantation (HIV-positive donor to HIV-positive recipient) is now performed in specialized centers and expands the donor pool. Post-transplant drug interactions between calcineurin inhibitors and boosted ARVs require careful management — cobicistat or ritonavir can elevate tacrolimus levels 10–100x via CYP3A4 inhibition; prefer unboosted INSTI-based regimens post-transplant whenever possible.

Section 8

Drug Interactions in CKD + HIV

Drug Pair Interaction Management
Cobicistat/ritonavir + tacrolimus CNI levels rise 10–100x (CYP3A4 inhibition) Prefer unboosted INSTI (DTG, RAL, BIC) post-transplant; if boosted ARV unavoidable: tacrolimus 0.5 mg/week + daily TDM
Rifampicin + DTG DTG levels fall ~75% (UGT1A1 induction) Double DTG to 50 mg twice daily; BIC contraindicated with rifampicin
TMP-SMX + TDF Raises creatinine (MATE1 artifact) + increases tenofovir levels Confirm GFR with cystatin C; switch TDF → TAF; avoid in CKD G4+
NSAIDs + TDF Synergistic nephrotoxicity Contraindicated — use paracetamol for analgesia
Cobicistat creatinine artifact +0.1–0.2 mg/dL rise in creatinine without true GFR decline (MATE1/2-K inhibition) Confirm with cystatin C before switching ARVs for apparent CKD progression
ⓘ

Cross-reference: ARV dose adjustment tables

See Module 14 of the CKD Prescriber's Playbook (medication-operational-guide.html) for complete ARV dose-adjustment tables by CrCl stage and HD/PD.

Section 9

Screening and Prevention

Who to Screen What to Check Frequency Action Threshold
All PLHIV at ART initiation Creatinine + eGFR, urine dipstick (protein), urine PCR Baseline Proteinuria 2+ or eGFR <60: nephrology referral
PLHIV on TDF Creatinine, eGFR, urine PCR, serum phosphate, urine glucose Every 6 months Glucosuria + hypophosphatemia: switch TDF → TAF immediately
Stable PLHIV on TAF/non-TDF ART Creatinine, eGFR, urine dipstick Annually eGFR decline >5 mL/min/year or new proteinuria: nephrology referral
High-risk PLHIV (CD4 <200, detectable VL, HTN, DM, prior AKI) Full panel: creatinine, eGFR, electrolytes, phosphate, urine PCR Every 3 months Any new proteinuria or eGFR decline: expedited nephrology referral
HIV testing in unexplained proteinuria HIV rapid test / HIV-1 RNA Once, with consent New HIV diagnosis: start ART; nephrology co-management
●

Primary prevention of HIVAN = early ART initiation

The most effective intervention is ensuring no PLHIV remains untreated. Universal ART regardless of CD4 count (per 2015 WHO guidelines) has dramatically reduced HIVAN incidence in countries with high ART coverage.

Section 10

Quick Reference Card

HIVAN & HIV Kidney Disease — Clinician Reference

  • HIVAN diagnosis: nephrotic proteinuria + enlarged echogenic kidneys + detectable HIV + CD4 <200 → start ART immediately
  • ART is first-line treatment — do not delay for biopsy in rapidly progressive HIVAN
  • Preferred regimen: DTG or BIC + TAF/FTC; avoid TDF in HIVAN, CrCl <50
  • ACEi or ARB: standard of care for proteinuria reduction; target BP <130/80
  • Corticosteroids: reserve for ART-unresponsive HIVAN; give PCP prophylaxis concurrently
  • Expect response: proteinuria improvement within 4–12 weeks of viral suppression
  • HIVICK: occurs at any CD4/VL; needs biopsy; management differs from HIVAN
  • TDF nephrotoxicity: glucosuria + hypophosphatemia + tubular proteinuria → stop TDF → TAF
  • Cobicistat creatinine artifact: confirm with cystatin C before switching ARVs
  • HIV is not a contraindication to dialysis or kidney transplant
  • Post-transplant: prefer unboosted INSTI — cobicistat/ritonavir causes tacrolimus toxicity
  • Screen all PLHIV at ART initiation: creatinine, eGFR, urine protein
Dr. W. G. M. Rivero

W. G. M. Rivero, MD, FPCP, DPSN

This clinician reference covers the full spectrum of HIV-related kidney disease with an emphasis on practical diagnosis and ART-based nephroprotection. Philippine context is integrated throughout for locally relevant decision-making.

Internal Medicine · Nephrology · Philippines · williamriveromd.com

Clinical Disclaimer: This guide is intended as a clinical reference and does not replace institutional protocols, specialist consultation, or current Philippine Society of Nephrology and PSMID guidelines. ARV dosing and drug interaction data should be verified against current prescribing information and the Lexicomp/Micromedex database. Evidence levels cited are consistent with KDIGO 2024 and current HIV medicine guidelines.

Related Guides

Nephrology Understanding CKD A complete guide to chronic kidney disease — what it is, how it progresses, and what you can do. → Clinician Reference The CKD Prescriber's Playbook Complete prescribing protocols for CKD and dialysis — includes ARV dose-adjustment tables by CrCl stage (Module 14). → Nephrology Proteins and Proteinuria Why protein in the urine matters, what the tests mean, and how to reduce protein loss. → Nephrology Slowing CKD Progression Evidence-based strategies to protect kidney function and delay the need for dialysis. → Nephrology Glomerulonephritis Understanding inflammation of the kidney's filtering units — types, causes, diagnosis, and treatment. →