Summative Revision Notes
These notes summarise the seven Morning Rounds in the Nephrology series. They are written for rapid pre-exam revision, not first-time learning. Each section is self-contained. Read the debrief panels in the quizzes for the full clinical reasoning — use these notes to consolidate, not to meet the topic for the first time.
| Stage | Creatinine (both systems) | Urine Output | RIFLE equivalent |
|---|---|---|---|
| KDIGO Stage 1 | ≥1.5× baseline or ≥0.3 mg/dL rise within 48 h | <0.5 mL/kg/h >6 h | Risk |
| KDIGO Stage 2 | ≥2.0× baseline | <0.5 mL/kg/h >12 h | Injury |
| KDIGO Stage 3 | ≥3.0× baseline or Cr ≥4.0 mg/dL or RRT initiated | <0.3 mL/kg/h ≥24 h or anuria ≥12 h | Failure |
| RIFLE only | Loss (>4 weeks); ESRD (>3 months) | — | Outcome stages |
Key KDIGO addition over RIFLE: the 0.3 mg/dL rise within 48 hours criterion for Stage 1. KDIGO dropped RIFLE's outcome stages (Loss, ESRD).
| Parameter | Pre-renal | ATN (Intrinsic) |
|---|---|---|
| FENa | <1% | >2% |
| Urine Na | <20 mEq/L | >40 mEq/L |
| Urine SG | >1.020 | ~1.010 (isosthenuria) |
| BUN:Cr ratio | >20:1 | ~10:1 |
| Urine microscopy | Normal / hyaline casts | Muddy brown granular casts |
| Response to fluids | Creatinine falls | Does not respond |
FENa caveat: falsely elevated (>1%) in pre-renal AKI if patient is on diuretics. Use FE-Urea (<35% = pre-renal) in patients on diuretics. FENa is also <1% in contrast nephropathy and myoglobinuria despite ATN.
Acidosis (pH <7.2 unresponsive to treatment) · Electrolytes (K⁺ >6.5 with ECG changes) · Intoxication (dialysable toxins) · Overload (pulmonary oedema refractory to diuretics) · Uraemia (encephalopathy, pericarditis, bleeding). Creatinine alone is never an absolute threshold.
Prevention: IV isotonic saline (1 mL/kg/h before and after) is the only evidence-based intervention. NAC: large RCTs (PRESERVE, ACT) showed no benefit over hydration — no longer routinely recommended. Iso-osmolar contrast reduces osmotic load but does not replace hydration.
FENa <1% = pre-renal Muddy brown casts = ATN KDIGO adds 0.3 mg/dL/48h NAC = no benefit (PRESERVE)
| Stage | eGFR (mL/min/1.73 m²) | Label | Albuminuria |
|---|---|---|---|
| G1 | ≥90 | Normal/High | A1 <30 mg/g (normal–mild) |
| G2 | 60–89 | Mildly decreased | |
| G3a | 45–59 | Mild–moderately decreased | A2 30–300 mg/g (moderate) |
| G3b | 30–44 | Moderately–severely decreased | A3 >300 mg/g (severe) |
| G4 | 15–29 | Severely decreased | |
| G5 | <15 | Kidney failure (ESRD) |
CKD requires abnormality persisting >3 months. G1A1 or G2A1 without structural abnormality does not constitute CKD.
Failing kidney → ↓1-alpha-hydroxylase → ↓1,25-OH Vitamin D → hypocalcaemia + phosphate retention → secondary HPT (↑PTH). First-line: dietary phosphate restriction + phosphate binders (sevelamer, calcium carbonate, lanthanum). Active Vitamin D analogues (calcitriol, alfacalcidol) for the 1,25-OH deficiency. Tertiary HPT = autonomous PTH secretion after prolonged secondary HPT; PTH stays high even after calcium corrected.
RAS blockade (ACEi or ARB): reduces intraglomerular pressure via efferent arteriolar dilation; first-line in diabetic nephropathy with proteinuria. SGLT2 inhibitors: renal protection independent of glycaemic effect — CREDENCE, DAPA-CKD, EMPA-KIDNEY trials. BP target in CKD with proteinuria: <130/80 mmHg. Dual RAS blockade (ACEi + ARB): contraindicated — ONTARGET trial showed increased AKI and hyperkalaemia, no additional benefit.
Before starting ESA: confirm iron stores adequate — TSAT >20% and ferritin >200 ng/mL (dialysis patients); >100 ng/mL (non-dialysis). IV iron preferred in dialysis (hepcidin blocks oral absorption). ESA targets: Hb 10–12 g/dL. Targeting >13 g/dL increases stroke and thrombosis (CHOIR, CREATE trials). ESA hyporesponsiveness: exclude iron deficiency, infection, aluminium toxicity, haemolysis, myeloma.
Early initiation (eGFR 10–14) vs late (eGFR 5–7): no survival advantage to early start. Initiate when uraemic symptoms, refractory fluid overload, or metabolic complications develop — not at a fixed eGFR threshold.
CKD >3 months + two measurements SGLT2i: CREDENCE, DAPA-CKD Dual RAS = contraindicated Hb ceiling 12 g/dL on ESA
| Feature | Nephrotic | Nephritic |
|---|---|---|
| Proteinuria | >3.5 g/day | <3.5 g/day |
| Haematuria | Absent/minimal | Prominent (RBC casts) |
| Hypertension | Usually absent initially | Present |
| Oedema mechanism | Hypoalbuminaemia | Sodium retention |
| Renal function | Normal early | ↑ Creatinine |
Linear IgG = anti-GBM Wire-loop = Lupus IV Anti-PLA2R = primary MGN Synpharyngitic = IgA nephropathy
| Type | Defect | Serum K⁺ | Urine pH | Stones/NCC | Classic causes |
|---|---|---|---|---|---|
| Type I (Distal) | ↓H⁺ secretion, collecting duct | ↓ Low | >5.5 always | Yes (Ca-PO₄) | Sjögren, SLE, amphotericin B, lithium |
| Type II (Proximal) | ↓HCO₃⁻ reabsorption | ↓ Low | Variable; can be <5.5 | Rare | Fanconi (Wilson, cystinosis, tenofovir, myeloma) |
| Type IV | ↓Aldosterone / resistance | ↑ High | ≤5.5 | No | DM (hyporeninism), ACEi/ARB, heparin, CKD |
All three RTAs: normal anion gap metabolic acidosis (NAGMA). Type I is the only one where urine pH cannot fall below 5.5 regardless of systemic acidosis. Type IV is the commonest RTA in adults.
All proximal tubular reabsorptates lost: glucose (normoglycaemic glycosuria), phosphate, uric acid, amino acids, potassium, bicarbonate. Mnemonic: GARBAGE. Causes: cystinosis (children), Wilson disease, tenofovir (TDF), ifosfamide, lead, multiple myeloma. Tenofovir mechanism: mitochondrial DNA polymerase gamma inhibition in proximal tubular cells. Switch to TAF (tenofovir alafenamide — less nephrotoxic).
Both: hypokalaemic metabolic alkalosis, normal BP, high renin/aldosterone, mimic diuretics. Bartter (thick ascending limb defect = furosemide-like): presents in infancy/childhood, hypercalciuria, nephrocalcinosis, polyuria. Gitelman (DCT defect = thiazide-like): presents in adults incidentally, hypomagnesaemia + hypocalciuria. Exam pivot: Bartter = Ca up; Gitelman = Ca down.
Lithium enters collecting duct principal cells via ENaC → inhibits adenylyl cyclase → ↓cAMP → AQP2 channels not inserted → tubule impermeable to water despite normal/high ADH. DDAVP test: no response (vs central DI where urine osmolality rises >50%). Paradoxical treatment: thiazides (mild volume depletion → ↑ proximal reabsorption → ↓ urine volume) + amiloride (blocks ENaC, ↓ lithium entry).
Type I RTA: urine pH >5.5 always Type IV: K⁺ high Bartter = hypercalciuria Gitelman = hypoMg + hypocalciuria
| Volume status | Urine Na | Diagnoses |
|---|---|---|
| Hypovolaemic | <20 mEq/L | GI/skin losses (vomiting, diarrhoea, burns) |
| Hypovolaemic | >20 mEq/L | Diuretics, adrenal insufficiency, RTA |
| Euvolaemic | >40 mEq/L | SIADH, hypothyroidism, polydipsia |
| Hypervolaemic | <20 mEq/L | CCF, cirrhosis, nephrotic syndrome |
SIADH criteria: true hypoosmolar hyponatraemia + urine osmolality >100 mOsm/kg + urine Na >40 + euvolaemic + normal thyroid/adrenal. Causes: SSRIs, carbamazepine, malignancy (SCLC), pulmonary/CNS disease. Treatment: fluid restriction first; hypertonic saline for symptomatic severe cases. Correction ceiling: 8 mEq/L in 24 h. Overcorrection → ODS (osmotic demyelination syndrome).
Always a free-water deficit. Formula: Water deficit = 0.6 × weight × [(Na/140) − 1]. Replace with 0.45% saline or 5% dextrose. Correction rate: no faster than 0.5 mEq/L/hour or 10–12 mEq/L/day. Rapid correction → cerebral oedema (brain has made idiogenic osmoles).
Calcium gluconate (membrane stabilisation, onset 1–3 min — first when ECG changes present) → Bicarbonate (if acidotic) → Dextrose-insulin (10 u actrapid + 50 mL 50% dextrose, lowers K by 0.5–1.5 mEq/L, onset 15–30 min) → Excretion (resonium, patiromer, SZC, loop diuretic) → RRT. Calcium does not lower K — it antagonises membrane depolarisation.
Hypokalaemia + hypertension + metabolic alkalosis + renal K wasting (UK:UCr elevated) + suppressed renin + elevated aldosterone = Primary Hyperaldosteronism. Workup: ARR (>30 with aldosterone >15 ng/dL) → confirmatory test → adrenal CT → adrenal vein sampling. Unilateral adenoma: adrenalectomy. Bilateral hyperplasia: spironolactone/eplerenone.
Urine Cl <20 mEq/L = chloride-responsive (saline-responsive): vomiting, nasogastric drainage, antacid excess, post-diuretic state. Treat with IV normal saline. Urine Cl >20 = chloride-resistant: primary hyperaldosteronism, Cushing — saline will not correct; treat the cause. Alkalosis → tetany from reduced ionised calcium (alkalosis increases protein binding).
ODS: >8 mEq/L/day overcorrection Ca gluconate first in hyperkalaemia Conn: suppressed renin + ↑ aldosterone Urine Cl classifies metabolic alkalosis
| Feature | Haemodialysis | Peritoneal Dialysis |
|---|---|---|
| Setting | Hospital/centre, 3×/week | Home (CAPD or APD) |
| Residual renal function | Lost faster (haemodynamic stress) | Better preserved |
| Solute clearance | More efficient per session (KT/V ≥1.2) | Continuous but lower per-session |
| Contraindications | Vascular access failure | Prior abdominal surgery/adhesions, herniae |
| Access | AV fistula (preferred), graft, CVC | Tenckhoff catheter |
Commonest HD complication (~20–30% sessions). Mechanism: UF rate exceeds plasma refilling. Management: stop UF, Trendelenburg, IV saline/hypertonic saline. Prevention: sodium profiling, cooled dialysate (35°C), UF rate limit <13 mL/kg/h, hold antihypertensives on dialysis day.
Diagnosis: effluent WBC >100/mm³ with >50% neutrophils. Commonest organism: coagulase-negative Staphylococcus. Treatment: intraperitoneal vancomycin + ceftazidime (empirical). Catheter removal: fungal peritonitis, refractory/relapsing peritonitis, faecal peritonitis, tunnel infection with peritonitis.
| Type | Timing | Mechanism | IF pattern | Treatment |
|---|---|---|---|---|
| Hyperacute | Minutes on table | Pre-formed anti-HLA Ab | Thrombosis, fibrin | Irreversible; nephrectomy |
| Acute Cellular | Wk 1–3 (peak) | CD8+ T-cell mediated | Tubulitis + interstitial infiltrate | Pulse IV methylprednisolone ×3d |
| Chronic | Months–years | T-cell + antibody | Fibrosis, intimal hyperplasia | Optimise IS; no reversal |
Hyperacute prevented by pre-transplant crossmatch. Standard triple IS: tacrolimus + MMF + prednisolone. Steroid-resistant acute rejection: ATG (anti-thymocyte globulin).
EBV-driven B-cell proliferation from immunosuppression-induced T-cell suppression. Presents months–years post-transplant. First step: reduction of immunosuppression (RIS) — stop MMF first. CD20+ disease not responding: rituximab. Aggressive disease: R-CHOP.
PD peritonitis: WBC >100 Hyperacute = pre-formed Ab ACR: pulse steroids PTLD: reduce IS first
| Feature | PKD1 (chromosome 16p) | PKD2 (chromosome 4q) |
|---|---|---|
| Frequency | ~85% | ~15% |
| Protein | Polycystin-1 | Polycystin-2 |
| ESRD median age | ~54 years | ~74 years |
| Severity | More severe | Milder |
| Inheritance | Autosomal dominant (1 in 400–1000) | |
Earliest manifestation: hypertension (↑intrarenal RAAS). Progression marker: total kidney volume (TKV) on MRI. Treatment: tolvaptan (V2-receptor antagonist slows TKV growth — TEMPO trial). Diagnosis by ultrasound: Ravine criteria (age-dependent cyst counts).
Extrarenal manifestations: intracranial berry aneurysms (5–10%, most feared — SAH), hepatic cysts (commonest, ~80% by age 60, usually benign), mitral valve prolapse (~25%), aortic root dilatation, pancreatic and seminal vesicle cysts. MRA brain screening: indicated if family history of SAH, high-risk occupation, prior aneurysm — not routine for all.
| Feature | Fibromuscular Dysplasia | Atherosclerotic RAS |
|---|---|---|
| Patient | Young women | Older, cardiovascular risk factors |
| Location | Mid/distal renal artery | Ostial/proximal |
| Angiography | String of beads | Smooth stenosis |
| Treatment | PTA alone (no stent) | Medical therapy (ASTRAL, CORAL trials — stenting no benefit) |
ACEi/ARB in RAS: contraindicated in bilateral RAS or RAS in a solitary kidney — loss of efferent arteriolar tone → acute GFR fall.
Severe BP + papilloedema (Grade IV retinopathy) + AKI + MAHA (schistocytes). Fibrinoid necrosis of arterioles → RAAS activation → vicious cycle. Treatment: IV antihypertensives (labetalol, nicardipine). Critical rule: reduce MAP by no more than 20–25% in the first hour. Rapid normalisation → cerebral/renal hypoperfusion (autoregulation reset). Renal function may transiently worsen before improving.
| Feature | STEC-HUS | TTP |
|---|---|---|
| Mechanism | Shiga toxin → endothelial injury | ADAMTS13 deficiency → ultra-large vWF |
| Trigger | E. coli O157:H7 (bloody diarrhoea) | Autoantibody to ADAMTS13 |
| Dominant organ | Kidney (AKI) | Brain (neuro symptoms) |
| Treatment | Supportive; avoid antibiotics | Plasma exchange (urgent) |
| Age/context | Children, food outbreak | Young women, idiopathic/drug |
Both: MAHA (schistocytes) + thrombocytopenia + negative Coombs. In STEC-HUS: antibiotics lyse bacteria → massive Shiga toxin release → worsens clinical course. Plasma exchange is not indicated in STEC-HUS; it is essential in TTP (ADAMTS13 <10%).
ADPKD berry aneurysm: screen if FHx SAH FMD: PTA no stent MAP: max 25% drop in 1st hour HUS: no antibiotics
For clinical reasoning practice, return to the seven Morning Rounds quizzes linked in the series index.