# Nephrotic vs Nephritic Syndrome: USMLE Chart

> What is the difference between nephrotic and nephritic syndrome?

How proteinuria, urine sediment and complement separate the two syndromes, with biopsy findings for 13 glomerular diseases, current KDIGO guidance and 2026 IgA nephropathy approvals.

Nephrotic syndrome is massive protein leak through a damaged glomerular filter: proteinuria above 3.5 g/day, serum albumin below 3.0 g/dL, edema, hyperlipidemia and fatty casts. Nephritic syndrome is inflammatory glomerular injury: dysmorphic red cells and RBC casts, usually subnephrotic proteinuria, hypertension, oliguria and rising creatinine. The sediment usually names the syndrome; complement then narrows the cause.

## What is the difference between nephrotic and nephritic syndrome?

The difference is the type of glomerular injury. In nephrotic syndrome the filtration barrier, chiefly the podocytes, fails, so albumin floods the urine, but inflammation is minimal and few red cells escape. In nephritic syndrome, antibodies, immune complexes or complement inflame the capillary wall, so dysmorphic red cells leak out and set into RBC casts in the tubules. Falling filtration then brings salt and water retention, hypertension, oliguria and a rising creatinine, while nephrotic edema is blamed on low oncotic pressure, primary renal sodium retention or both. More comparisons sit on the [Nephrology](/topics/nephrology) hub.

| Feature | Nephrotic syndrome | Nephritic syndrome |
| --- | --- | --- |
| Main lesion | Podocyte or basement membrane damage, little inflammation | Inflamed glomerular capillaries |
| Proteinuria | Above 3.5 g/day (UPCR above 3,000 mg/g) | Usually below 3.5 g/day |
| Serum albumin | Below 3.0 g/dL | Normal or mildly low |
| Urine sediment | Fatty casts, oval fat bodies, Maltese crosses | Dysmorphic RBCs, RBC casts |
| Edema | Generalized; low oncotic pressure and/or renal sodium retention | Salt and water retention |
| Blood pressure | Often normal | Usually raised |
| Creatinine | Often normal at onset | Often rising, with oliguria |
| Complement | Usually normal | Low in PSGN, lupus, MPGN, C3G; usually normal in IgAN, anti-GBM, ANCA GN |
| Classic causes | MCD, FSGS, membranous, diabetic, amyloid | PSGN, IgAN, anti-GBM, ANCA GN, Alport |

Lupus nephritis (nephritic in classes III and IV, nephrotic in class V) and MPGN-pattern disease can mix both pictures.

## How the labs define each syndrome

KDIGO 2021 defines adult nephrotic syndrome as proteinuria above 3.5 g/day (UPCR above 3,000 mg/g, or 300 mg/mmol) plus serum albumin below 3.0 g/dL, often but not necessarily with edema and dyslipidemia; heavy proteinuria with a normal albumin is nephrotic-range proteinuria, not the syndrome. For children, KDIGO 2025 sets nephrotic-range proteinuria at a UPCR of at least 2 g/g (200 mg/mmol) or 3+ to 4+ on dipstick, and steroid-sensitive disease means complete remission within 4 weeks of standard-dose prednisone or prednisolone. A nephritic sediment has more than 5 RBCs per high-power field with dysmorphic forms, often with RBC casts. RPGN means kidney function lost over days to weeks, usually with crescents in half or more of sampled glomeruli.

## Biopsy findings, disease by disease

Each disease has a signature on light, immunofluorescence and electron microscopy, plus a typical patient.

**Nephrotic-pattern diseases**

| Disease | Light microscopy | Immunofluorescence | Electron microscopy | Classic patient | Treatment |
| --- | --- | --- | --- | --- | --- |
| Minimal change disease | Normal | Negative | Diffuse foot-process effacement | Young child; adult on NSAIDs or with Hodgkin lymphoma | Glucocorticoids; steroid-sparing drugs for relapses |
| FSGS | Segmental sclerosis; collapsing variant in HIV | Nonspecific IgM and C3 in scarred segments | Effacement, diffuse if primary, patchy if secondary | Black adult; HIV, heroin, obesity, APOL1 variants | Primary: glucocorticoids, calcineurin inhibitor if resistant; secondary: treat the cause |
| Membranous nephropathy | Thick capillary walls; silver-stain spikes | Granular IgG (IgG4 if primary) and C3 | Subepithelial deposits | Adult in their 50s; anti-PLA2R; hepatitis B, lupus, solid tumor, NSAIDs | By risk: supportive care, rituximab, cyclophosphamide plus glucocorticoids, or a calcineurin inhibitor |
| Diabetic nephropathy | Mesangial expansion, Kimmelstiel-Wilson nodules, hyaline arteriolosclerosis of both arterioles | Not diagnostic | GBM thickening | Long-standing diabetes with retinopathy; albuminuria of 30-300 mg/day first | ACE inhibitor or ARB; add an SGLT2 inhibitor in type 2 diabetes |
| Amyloidosis | Congo red, apple-green birefringence under polarized light | Clonal light chain in AL | Nonbranching 10-nm fibrils | Myeloma (AL); rheumatoid arthritis, IBD, familial Mediterranean fever (AA) | Treat the clone (AL) or the inflammation (AA) |
| Lupus nephritis, class V | Thick capillary loops | IgG, IgA, IgM and complement | Subepithelial deposits | Woman with SLE and nephrotic syndrome | Hydroxychloroquine plus immunosuppression |

**Nephritic and mixed-pattern diseases**

| Disease | Light microscopy | Immunofluorescence | Electron microscopy | Classic patient | Treatment |
| --- | --- | --- | --- | --- | --- |
| Post-streptococcal GN | Hypercellular glomeruli | Granular IgG and C3 ("starry sky") | Subepithelial humps | Child aged 3-15 after strep throat or impetigo; low C3 | Supportive; penicillin to clear strep |
| IgA nephropathy | Mesangial hypercellularity | Mesangial IgA with C3 | Mesangial deposits | Young man with gross hematuria 1-2 days into a URI | See the IgAN section below |
| Anti-GBM disease | Crescents | Linear IgG along the GBM | -- | Smoker with hemoptysis | Plasma exchange, glucocorticoids, cyclophosphamide |
| Pauci-immune ANCA GN | Necrotizing crescents | Few or no deposits | Few or no deposits | GPA (sinusitis, lung nodules, PR3-ANCA); MPA (MPO-ANCA) | Glucocorticoids plus rituximab or cyclophosphamide |
| Lupus nephritis, class III or IV | Focal or diffuse proliferation; wire loops | IgG, IgA, IgM and complement | Subendothelial deposits | Young woman with SLE, low C3 and C4, anti-dsDNA | Hydroxychloroquine, glucocorticoids plus MMF or cyclophosphamide; add-on belimumab, voclosporin or obinutuzumab |
| Immune-complex MPGN | GBM double contours ("tram-track") | IgG or IgM with C3 | Subendothelial deposits | Hepatitis C cryoglobulinemia, hepatitis B, lupus; low C4 | Treat the cause; pegcetacoplan for primary disease (age 12+) |
| C3 glomerulopathy | MPGN pattern | C3-dominant | Ribbon-like dense deposits (dense deposit disease) | Often a child or adolescent; C3 nephritic factor; low C3, normal C4 | Iptacopan (adults) or pegcetacoplan (age 12+) |
| Alport syndrome | Normal early, later sclerosis | Negative; collagen IV alpha chains absent on special stains | GBM splitting and lamellation | Boy with hematuria, hearing loss, anterior lenticonus | Early ACE inhibitor or ARB |

Deep dives: [lupus nephritis classes](/blog/2026-06-02-q-bank-breakdown-lupus-nephritis-why-every-answer-choice-matters) and [crescentic RPGN types](/blog/2026-06-02-everything-you-need-to-know-about-rapidly-progressive-gn-crescentic-for-step-1).

## Serum complement splits the nephritic differential

Complement is the fastest serologic fork in a nephritic stem.

| Pattern | Diseases | Mechanism |
| --- | --- | --- |
| Low C3, C4 normal or near-normal | PSGN, C3 glomerulopathy | Alternative pathway |
| Low C4, C3 low or normal | Lupus nephritis, immune-complex MPGN including hepatitis C cryoglobulinemia | Classical pathway |
| Low, infection-linked | Endocarditis-associated GN, shunt nephritis | Persistent immune complexes |
| Usually normal | IgA nephropathy, IgA vasculitis, anti-GBM disease, ANCA GN | Immunofluorescence decides |

PSGN complement usually recovers within 6-8 weeks; a C3 that stays low suggests C3 glomerulopathy.

## Why nephrotic patients clot, get infected and run high lipids

Nephrotic urine carries away far more than albumin.

- **Clots.** Urinary antithrombin III loss, lower protein S and plasminogen and more prothrombotic factors cause DVT, pulmonary embolism and renal vein thrombosis, and membranous nephropathy carries a particularly high risk. KDIGO weighs low albumin against bleeding risk before preventive anticoagulation in membranous disease.
- **Infection.** Urinary loss of IgG and complement factors weakens opsonization of encapsulated bacteria, and nephrotic children with ascites can develop spontaneous bacterial peritonitis; KDIGO advises pneumococcal vaccination.
- **Lipids.** Increased hepatic lipoprotein synthesis raises cholesterol and triglycerides; consider a statin if dyslipidemia persists.
- **Acid-base.** Low albumin lowers the measured anion gap, so correct it first, as in the [acid-base approach](/blog/how-to-approach-acid-base-questions-usmle).

## IgA nephropathy: the most common primary GN worldwide

IgA nephropathy (Berger disease) is the most common primary glomerulonephritis worldwide, seen in about 1 in 10 US kidney biopsies and up to 40% in East Asia. It peaks in the second and third decades, men outnumber women about 2.5 to 1 in the US and Europe, and about 1 in 5 patients reaches kidney failure within 10 years.

**Four hits drive it:** excess galactose-deficient IgA1, autoantibodies against it, circulating immune complexes, and mesangial deposition that activates complement and inflammation.

**Presentation.** Synpharyngitic hematuria is visible blood in the urine during, or within 1-2 days of, a mucosal infection such as a sore throat, often recurring; others have persistent microscopic hematuria and proteinuria. Complement is usually normal. PSGN instead follows pharyngitis by about 1-3 weeks (CDC cites about 10 days) and impetigo by up to about 6 weeks, with a low C3; ASO rises in most patients after throat infection but less consistently after impetigo, and anti-DNase B also helps confirm recent strep.

**IgA vasculitis** (Henoch-Schönlein purpura) is the systemic form, mostly in children: palpable purpura on the buttocks and legs, arthralgias, abdominal pain, and nephritis in about 20-55% of affected children. KDIGO 2025 recommends against glucocorticoids to prevent nephritis in isolated extrarenal disease.

**Diagnosis.** Only a biopsy diagnoses IgAN, and KDIGO 2025 suggests considering one in adults with proteinuria of 0.5 g/day or more. The Oxford MEST-C score grades mesangial (M) and endocapillary (E) hypercellularity, segmental sclerosis (S), tubular atrophy/interstitial fibrosis (T) and crescents (C); combined with clinical data in the International IgAN Prediction Tool, it estimates risk but does not choose the drug.

**Treatment.** KDIGO's September 2025 guideline targets IgA immune-complex formation and the consequences of nephron loss at the same time. Proteinuria of 0.5 g/day or more, on or off treatment, marks risk of progression; the goal is below 0.5 g/day, ideally below 0.3.

| Option (US brand) | Target | US status, October 2026 | KDIGO position |
| --- | --- | --- | --- |
| ACE inhibitor or ARB | Angiotensin system | Generic | All patients, maximum tolerated dose (1B) |
| Sparsentan (Filspari) | Endothelin-A and angiotensin II receptors | Full approval | Replaces, not adds to, RAS blockade (2B) |
| SGLT2 inhibitor | Nephron protection | No IgAN-specific label | For patients at risk (2B) |
| Targeted-release budesonide (Tarpeyo) | Gut mucosal B cells making galactose-deficient IgA1 | Full approval | 9-month course (2B) |
| Iptacopan (Fabhalta) | Complement factor B | Label changed July 2026 to slowing kidney function decline | Commentary: anti-inflammatory (hit 4) |
| Atrasentan (Vanrafia) | Endothelin-A receptor | Accelerated approval, April 2025 | Similar slot to sparsentan, but added to RAS blockade |
| Sibeprenlimab (Voyxact) | APRIL | Accelerated approval, November 2025 | Cuts pathogenic IgA (hits 1-3) |
| Atacicept (Trutakna) | APRIL and BAFF | Accelerated approval, July 2026 | Cuts pathogenic IgA (hits 1-3) |

Accelerated approvals rest on proteinuria, so kidney-function benefit is not yet established, and KDIGO's March 2026 commentary makes no formal recommendations on them. Boxed warnings: sparsentan for hepatotoxicity (with a REMS) and embryo-fetal toxicity, atrasentan for embryo-fetal toxicity, iptacopan for serious infections with encapsulated bacteria (with a REMS). Rapidly progressive IgAN gets cyclophosphamide and glucocorticoids.

## Antibodies that are reshaping the nephrotic workup

Anti-PLA2R antibodies mark about 70-80% of primary membranous nephropathy, and anti-THSD7A another 1-5%. KDIGO 2021 says a biopsy is no longer required to confirm membranous nephropathy in nephrotic syndrome with a positive PLA2R test; titers track treatment response, and secondary causes still need excluding.

Anti-nephrin antibodies target a podocyte slit-diaphragm protein. A 2024 multicenter study found them in 44% of adults with minimal change disease and 52% of children with idiopathic nephrotic syndrome (69% and 90% when untreated and active), and KDIGO's 2025 pediatric guideline cites that work. Testing was not yet widely available in 2025, so exams still expect a steroid trial in a child and a biopsy in an adult.

## A stepwise workup

Run every glomerular stem in the same order.

1. **Urinalysis with microscopy** names the syndrome.
2. **Spot UPCR** quantifies protein; check creatinine, albumin, C3 and C4.
3. **Serology.** Nephritic: ASO or anti-DNase B, ANA and anti-dsDNA, ANCA, anti-GBM, hepatitis B and C, cryoglobulins. Nephrotic: anti-PLA2R, HbA1c, ANA, hepatitis B and C, HIV.
4. **Biopsy** unexplained adult nephrotic syndrome, an active sediment and steroid-resistant children (with genetic testing considered). Skip it in typical childhood steroid-sensitive disease and classic PSGN; it is optional with PLA2R-positive nephrotic syndrome, and in diabetes it is reserved for rapid GFR decline, absent retinopathy, short duration, RBC casts or sudden nephrotic syndrome.

## KDIGO guideline map and shared supportive care

Supportive care is shared: an ACE inhibitor or ARB, sodium below 2 g/day, loop diuretics, statins and anticoagulation for thromboembolism. Immunosuppression follows the current KDIGO chapter:

- **2021 Glomerular Diseases:** membranous, adult MCD and FSGS, infection-related GN, anti-GBM and MPGN-pattern disease; KDIGO is replacing it chapter by chapter.
- **2024:** Lupus Nephritis (January) and ANCA-Associated Vasculitis (March).
- **2025:** Nephrotic Syndrome in Children (April; 8 or 12 weeks of initial glucocorticoids) and IgAN/IgAV (September), plus the 2026 IgAN commentary.

## How USMLE tests it: patterns and traps

Stems usually hinge on one discriminator: age, latency, complement or an exposure.

- **Child with periorbital edema, 4+ protein and no blood:** minimal change disease; steroids, no biopsy.
- **Adult in their 50s with anti-PLA2R, then sudden flank pain:** membranous nephropathy with renal vein thrombosis.
- **Diabetes with retinopathy and albuminuria:** Kimmelstiel-Wilson nodules; a high potassium may add type 4 [RTA](/blog/renal-tubular-acidosis-types-usmle).
- **Hematuria 1-2 days into a URI with normal C3:** IgA nephropathy, not PSGN, which needs a latent period of 1-3 weeks and lowers C3.
- **Hemoptysis with linear IgG:** anti-GBM disease; pauci-immune staining with sinusitis and lung nodules is GPA.
- **Trap: expecting low complement in anti-GBM or ANCA GN.** Both usually keep it normal.
- **Trap: diagnosing IgAN from serum IgA.** Only a biopsy counts.

> **10-second exam strategy:** Sediment first: fatty casts -> nephrotic, RBC casts -> nephritic. Nephrotic: child -> minimal change; HIV, heroin or Black adult -> FSGS; PLA2R or hepatitis B -> membranous; myeloma -> amyloid. Nephritic: low C3 -> PSGN, lupus or MPGN/C3G; normal C3 -> IgA, anti-GBM or ANCA. Creatinine rising over days to weeks -> crescents; read the immunofluorescence.

## Worked vignette

A 21-year-old man has cola-colored urine that began 36 hours after a sore throat started; he had a similar episode last winter. Blood pressure is 132/80 mm Hg, hearing and eye examinations are normal, and no relative has kidney disease. Urine shows dysmorphic red cells, 24-hour protein is 1.2 g, C3 and C4 are normal and creatinine is 1.0 mg/dL. A kidney biopsy is most likely to show:

- **A.** Subepithelial humps with granular IgG and C3
- **B.** Mesangial IgA deposits with mesangial hypercellularity
- **C.** Linear IgG along the glomerular basement membrane
- **D.** Normal glomeruli with diffuse foot-process effacement
- **E.** Splitting and lamellation of the glomerular basement membrane

**Answer: B.** Hematuria within 1-2 days of an infection, a prior episode and normal complement point to IgA nephropathy. **A** (PSGN) follows pharyngitis by 1-3 weeks and lowers C3. **C** (anti-GBM) drives creatinine up over days to weeks, often with hemoptysis. **D** (minimal change disease) presents with nephrotic syndrome, not gross hematuria. **E** (Alport syndrome) can flare with infections but usually brings hearing loss, eye findings and a family history.

**Next step:** with IgAN confirmed and proteinuria of 1.2 g/day, KDIGO 2025 counts him at risk: give a maximally tolerated ACE inhibitor or ARB (or sparsentan in its place), consider an SGLT2 inhibitor and targeted-release budesonide, and aim below 0.5 g/day.

## Sources

- KDIGO: [guidelines](https://kdigo.org/guidelines/), [2021 GN page](https://kdigo.org/guidelines/gd/), [2021 summary](https://kdigo.org/wp-content/uploads/2017/02/KDIGO-2021-GD-Guideline-Executive-Summary.pdf), [2021 full text](https://kdigo.org/wp-content/uploads/2024/05/KDIGO-2021-Glomerular-Diseases-Guideline_English_2024-Chapter-Updates.pdf), [membranous takeaways](https://kdigo.org/wp-content/uploads/2017/02/KDIGO-GD-Guideline-Key-Takeaways-for-Clinicians-Membranous-Nephropathy.pdf), [MCD takeaways](https://kdigo.org/wp-content/uploads/2017/02/KDIGO-GD-Guideline-Key-Takeaways-for-Clinicians-Minimal-Change-Disease.pdf), [IgAN 2025 page](https://kdigo.org/guidelines/iga-nephropathy/), [IgAN summary](https://kdigo.org/wp-content/uploads/2025/09/KDIGO-2025-IgAN-IgAV-Guideline-Executive-Summary.pdf), [IgAN takeaways](https://kdigo.org/wp-content/uploads/2024/08/KDIGO-2025-IgAN-IgAV-Guideline-Key-Takeaways_IgAN.pdf), [2026 IgAN commentary](https://kdigo.org/wp-content/uploads/2026/09/KDIGO-IgAN-Commentary-Complement-Inhibitors-B-Cell-Modifying-Agents.pdf), [children 2025 guideline](https://kdigo.org/wp-content/uploads/2025/04/KDIGO-2025-Guideline-for-Nephrotic-Syndrome-in-Children.pdf)
- StatPearls (NCBI Bookshelf): [nephrotic syndrome](https://www.ncbi.nlm.nih.gov/books/NBK470444/), [nephritic syndrome](https://www.ncbi.nlm.nih.gov/books/NBK562240/), [glomerulonephritis](https://www.ncbi.nlm.nih.gov/books/NBK560644/), [minimal change](https://www.ncbi.nlm.nih.gov/books/NBK560639/), [FSGS](https://www.ncbi.nlm.nih.gov/books/NBK532272/), [membranous](https://www.ncbi.nlm.nih.gov/books/NBK559169/), [diabetic nephropathy](https://www.ncbi.nlm.nih.gov/books/NBK534200/), [lupus nephritis](https://www.ncbi.nlm.nih.gov/books/NBK499817/), [infection-related GN](https://www.ncbi.nlm.nih.gov/books/NBK538255/), [IgA nephropathy](https://www.ncbi.nlm.nih.gov/books/NBK538214/), [IgA vasculitis](https://www.ncbi.nlm.nih.gov/books/NBK537252/), [Goodpasture](https://www.ncbi.nlm.nih.gov/books/NBK459291/), [RPGN](https://www.ncbi.nlm.nih.gov/books/NBK557430/), [crescentic GN](https://www.ncbi.nlm.nih.gov/books/NBK430727/), [Alport](https://www.ncbi.nlm.nih.gov/books/NBK470419/)
- [Anti-nephrin review, Clinical Kidney Journal 2025](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12059633/)
- CDC: [post-streptococcal GN](https://www.cdc.gov/group-a-strep/hcp/clinical-guidance/post-streptococcal-glomerulonephritis.html); NIDDK: [IgA nephropathy](https://www.niddk.nih.gov/health-information/kidney-disease/iga-nephropathy), [nephrotic syndrome in adults](https://www.niddk.nih.gov/health-information/kidney-disease/nephrotic-syndrome-adults), [amyloidosis](https://www.niddk.nih.gov/health-information/kidney-disease/amyloidosis)

Drill sediment, complement and immunofluorescence until the split is instant: [Practice nephrotic vs nephritic questions on StepGenie](https://dashboard.stepgenie.app/sign-up).

## Frequently asked questions

### How much proteinuria defines nephrotic syndrome?

In adults, KDIGO defines nephrotic syndrome as proteinuria above 3.5 g per day, or a urine protein-to-creatinine ratio above 3,000 mg/g, plus serum albumin below 3.0 g/dL; edema and hyperlipidemia usually accompany it but are not required. For children, KDIGO 2025 sets nephrotic-range proteinuria at a ratio of at least 2 g/g (200 mg/mmol) or 3+ to 4+ on dipstick. Heavy proteinuria with a normal albumin is nephrotic-range proteinuria, not the full syndrome.

### How do you tell IgA nephropathy from post-streptococcal glomerulonephritis?

Timing and complement separate them. IgA nephropathy causes visible hematuria during or within 1 to 2 days of a sore throat or other mucosal infection, keeps a normal C3 and often recurs. Post-streptococcal glomerulonephritis follows strep pharyngitis after a latent period of about 1 to 3 weeks, or impetigo after up to about 6 weeks, lowers C3 until it recovers within 6 to 8 weeks, and shows subepithelial humps on electron microscopy.

### Which glomerular diseases cause low serum complement?

Low C3 with a normal or near-normal C4 points to alternative-pathway activation, as in post-streptococcal glomerulonephritis and C3 glomerulopathy. A low C4 points to classical-pathway activation by immune complexes, as in lupus nephritis, where C3 and C4 are typically both low, and in immune-complex membranoproliferative glomerulonephritis such as hepatitis C cryoglobulinemia. Endocarditis-associated nephritis also lowers complement. IgA nephropathy, anti-GBM disease and pauci-immune ANCA glomerulonephritis usually keep normal complement.

### Which drugs are FDA-approved for IgA nephropathy in 2026?

As of October 2026, delayed-release budesonide (Tarpeyo) and sparsentan (Filspari) have full approval, and the label for iptacopan (Fabhalta) was changed in July 2026 to slowing kidney function decline. Atrasentan (Vanrafia, April 2025), sibeprenlimab (Voyxact, November 2025) and atacicept (Trutakna, July 2026) hold accelerated approval based on proteinuria reduction. KDIGO 2025 still builds care on a maximized ACE inhibitor or ARB, or sparsentan in its place, plus an SGLT2 inhibitor for patients at risk.

### Why are patients with nephrotic syndrome prone to blood clots?

Nephrotic patients lose antithrombin III in the urine, have lower protein S and plasminogen levels and make more prothrombotic factors, so the blood tips toward clotting. Deep vein thrombosis, pulmonary embolism and renal vein thrombosis follow, and membranous nephropathy carries a particularly high risk. Renal vein thrombosis is often silent but can cause flank pain and hematuria. KDIGO weighs low serum albumin against bleeding risk when deciding on preventive anticoagulation in membranous nephropathy.

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Canonical page: [Nephrotic vs Nephritic Syndrome: USMLE Chart](https://www.stepgenie.app/blog/nephrotic-vs-nephritic-syndrome-usmle)
Topic hub: [Nephrology](https://www.stepgenie.app/topics/nephrology)