Eduovisual
Renal & Urinary
Hypertensive nephrosclerosis: management
— Histologic hallmarks: hyaline arteriolosclerosis, fibrointimal thickening of interlobular arteries, global glomerulosclerosis, tubular atrophy
— Often a clinical diagnosis of exclusion — biopsy rarely performed unless features atypical
— Long-standing HTN (typically >5–10 years), often poorly controlled or untreated
— Black patients at disproportionately higher risk; APOL1 high-risk genotypes accelerate progression
— Older adults, men > women, comorbid LVH, retinopathy, or PAD
— Second leading cause of ESRD in the US after diabetic nephropathy
— Slowly progressive eGFR decline (1–3 mL/min/yr if BP uncontrolled)
— Mild proteinuria (usually <1 g/day; nephrotic-range argues against it)
— Bland urine sediment — no active cellular casts
— Bilateral small, smooth kidneys on imaging in advanced disease
— Middle-aged or older patient with chronic HTN, modest proteinuria, slowly rising creatinine, no diabetes, normal complement, negative serologies
— LVH on ECG/echo and hypertensive retinopathy reinforce the diagnosis
Board pearl: If a hypertensive patient presents with proteinuria >1.5 g/day, hematuria with dysmorphic RBCs/casts, or rapid GFR decline, do not anchor on hypertensive nephrosclerosis — pursue glomerulonephritis workup (ANA, ANCA, complements, hepatitis serologies, SPEP, anti-GBM) and consider renal biopsy. Hypertensive nephrosclerosis is bland, slow, and proportionate to BP burden.
Step 3 management: Frame this as a longitudinal outpatient diagnosis — confirm chronicity, document end-organ damage, rule out secondary HTN and alternative renal pathology before committing to the label.
— 55–75-year-old with decade-plus history of HTN, often with intermittent medication adherence
— Discovered incidentally on routine labs: rising creatinine, eGFR 30–60, dipstick 1+ protein
— Asymptomatic until late stages (uremia, volume overload)
— BP history: age at diagnosis, peak readings, number/classes of agents, adherence, home BP logs
— Family history: HTN, ESRD, APOL1-associated nephropathy, polycystic kidney disease
— Diabetes screen: duration, A1c trend (DM nephropathy is the #1 mimic)
— NSAID, herbal, cocaine, methamphetamine, lithium use — chronic interstitial injury or accelerated HTN
— OSA symptoms (snoring, witnessed apneas) — reversible secondary HTN driver
— Symptoms of secondary HTN: spells (pheo), proximal weakness/hypokalemia (hyperaldosteronism), flash pulmonary edema (RAS), abdominal bruit
— Sudden BP rise in previously controlled patient → RAS, glomerulonephritis
— Hematuria, edema, frothy urine → glomerular disease
— B-symptoms, sinusitis, hemoptysis → ANCA vasculitis
— Onset <30 or >55 with no prior HTN → secondary HTN workup
— Salt intake, alcohol, tobacco, exercise, occupational stressors
— Insurance/medication access (prescription costs drive nonadherence and accelerated CKD)
— Cognitive status and caregiver support — predicts adherence and dialysis readiness later
Key distinction: Hypertensive nephrosclerosis develops over years; malignant nephrosclerosis develops over days–weeks with BP often >180/120, papilledema, MAHA, and AKI — entirely different urgent management pathway.
Step 3 management: At the index outpatient visit, document a structured BP history, confirm with home or ambulatory monitoring, and order baseline labs before assigning the diagnosis. Ambulatory BP monitoring (ABPM) catches masked HTN and white-coat HTN that would otherwise mislead therapy.
— Use validated oscillometric device, appropriate cuff size, seated 5 min, feet flat, arm at heart level, average ≥2 readings
— Check both arms initially; >15 mmHg difference suggests subclavian stenosis/aortic disease
— Orthostatics in elderly, diabetics, and those on multiple antihypertensives — guides target individualization
— Confirm office HTN with home BP monitoring (HBPM) or ABPM before escalating therapy
— Funduscopy: AV nicking, arteriolar narrowing, copper/silver wiring (chronic changes); flame hemorrhages, cotton-wool spots, papilledema → malignant phase
— Cardiac: sustained PMI, S4 gallop (LV hypertrophy/diastolic dysfunction), S3 if decompensated
— Vascular: carotid/abdominal/femoral bruits (suggest atherosclerosis ± RAS), diminished pedal pulses, AAA on palpation
— Volume status: JVP, lung crackles, lower-extremity edema — drives diuretic decisions
— Abdominal bruit with diastolic component → renal artery stenosis
— Palpable flank masses → ADPKD
— Rash, arthritis, oral ulcers → lupus nephritis
— Saddle-nose, nasal crusting → GPA
— Café-au-lait, neurofibromas → pheochromocytoma in NF1
— Truncal obesity, striae, proximal weakness → Cushing
— Pulse pressure widening in elderly = isolated systolic HTN with stiff vasculature — common substrate for nephrosclerosis
— Resting tachycardia: hyperadrenergic state, anemia of CKD, or thyrotoxicosis
Board pearl: In a chronic hypertensive patient, LVH on ECG (Sokolow-Lyon, Cornell) plus hypertensive retinopathy plus bilateral small kidneys on US is a near-pathognomonic triad for hypertensive nephrosclerosis — biopsy unnecessary.
Step 3 management: Document end-organ damage at baseline; it changes risk stratification (ASCVD ≥10%), determines statin initiation, and justifies aggressive BP targets.
— BMP: creatinine, eGFR (use 2021 CKD-EPI race-free equation), K, HCO₃, Na, glucose
— Cystatin C-based eGFR when muscle mass is atypical (elderly, sarcopenic, amputee, bodybuilder) — confirms staging
— CBC: anemia of CKD (normocytic, normochromic) appears at eGFR <60
— UA with microscopy: bland sediment expected; dysmorphic RBCs/RBC casts → glomerulonephritis; WBC casts → interstitial nephritis
— Urine albumin-creatinine ratio (UACR) on spot first-morning sample — typically <300 mg/g in nephrosclerosis; >300 mg/g should prompt reconsideration
— Lipid panel, HbA1c, fasting glucose — rule out diabetic nephropathy and quantify ASCVD risk
— Plasma aldosterone-to-renin ratio (ARR) if hypokalemia, resistant HTN, or HTN <30
— Plasma/urine metanephrines if spells, labile BP
— TSH, 24-hr urine cortisol or 1-mg dexamethasone suppression if clinical suspicion
— Renal duplex US if suspicion for RAS (flash pulmonary edema, AKI on ACEi, asymmetric kidneys)
— Renal ultrasound is first-line: bilateral small (<9 cm), smooth, echogenic kidneys with thinned cortex = chronic disease
— Asymmetry (>1.5 cm difference) → renovascular disease
— Cysts, hydronephrosis, stones → alternative diagnoses
— 12-lead ECG for LVH, prior MI, conduction disease
— TTE if LVH on ECG or HF symptoms — quantifies LV mass, diastolic dysfunction, EF (informs HFpEF management)
Board pearl: Bilateral small kidneys = chronic, generally non-reversible disease, and biopsy is contraindicated (high bleeding risk, low yield). Diagnose clinically.
Step 3 management: Stage CKD by eGFR + albuminuria (KDIGO heat map) at the first visit — this single act drives nephrology referral timing, drug dosing, ASCVD prevention intensity, and dialysis access planning years ahead.
— Atypical features: rapid eGFR decline (>5 mL/min/yr), nephrotic proteinuria, active sediment, systemic symptoms, age <30, no clear HTN history
— Discordant imaging (asymmetry, masses, obstruction)
— Failure to respond to optimized BP control
— ANA, anti-dsDNA, complements C3/C4 — lupus
— ANCA (PR3, MPO) — vasculitis
— Anti-GBM — Goodpasture
— Hepatitis B/C, HIV — secondary GN, HIVAN
— SPEP/UPEP with immunofixation, serum free light chains — myeloma, amyloid (especially older patients)
— Cryoglobulins if HCV positive or purpura
— Renal artery duplex US — operator-dependent; PSV >180 cm/s suggests stenosis
— CT angiography — high sensitivity; requires contrast (caution at eGFR <30; modern iso-osmolar contrast acceptable with hydration)
— MRA without gadolinium or with macrocyclic agents if eGFR <30 (NSF risk historically with older gadolinium)
— Captopril renography — largely obsolete
— Atypical presentation as above
— Kidneys still normal-sized
— Will change management (e.g., diagnose vasculitis warranting immunosuppression)
— Avoid in bilateral small kidneys, uncontrolled HTN, bleeding diathesis, single kidney
— APOL1 testing is becoming clinically available for African-ancestry patients with FSGS-like presentations; influences prognosis and emerging therapeutics (e.g., inaxaplin trials)
Key distinction: A rapidly rising creatinine after starting an ACEi/ARB (>30% in 1–2 weeks) raises bilateral renal artery stenosis — get duplex/CTA before reflexively stopping the agent permanently; mild expected bumps (≤30%) reflect intrarenal hemodynamics and are acceptable.
Step 3 management: Refer to nephrology when eGFR <30, UACR >300 mg/g, rapid decline, or diagnostic uncertainty. Early referral reduces emergency dialysis starts and improves modality choice.
— Slow CKD progression via BP and proteinuria control
— Reduce cardiovascular events (leading cause of death in CKD before reaching ESRD)
— Prepare for renal replacement when eGFR trajectory predicts ESRD within 1–2 years
— ACC/AHA 2017 and KDIGO 2021: target SBP <120 mmHg by standardized office measurement in most adults with CKD, when tolerated
— Individualize: frail elderly, orthostatic hypotension, high fall risk → <130/80 is reasonable
— Confirm with HBPM (target <125/75 home equivalent)
— SPRINT trial: intensive control (<120) reduced CV events and all-cause mortality in non-diabetic high-risk adults including CKD subgroup
— Reduce UACR by ≥30%, ideally to <300 mg/g; renoprotection tracks with proteinuria reduction independent of BP
— DASH diet, sodium <2.3 g/day (ideally 1.5 g), weight loss to BMI <25
— Aerobic exercise 90–150 min/week
— Alcohol ≤2 drinks/day men, ≤1 women
— Smoking cessation — independently accelerates CKD
— Avoid NSAIDs, decongestants, high-dose acetaminophen abuse, nephrotoxic herbals
— Kidney Failure Risk Equation (Tangri): 4- or 8-variable; 2-year and 5-year ESRD risk → guides nephrology referral, transplant evaluation, access planning
— ASCVD risk calculator for statin decisions
— KDIGO heat map for monitoring frequency
Step 3 management: Choose BP target collaboratively, document shared decision-making, and use HBPM logs to titrate. If a 70-year-old has orthostatic symptoms at SBP 118, accept 130 — board questions reward individualized targets over rigid numbers.
Board pearl: Most patients with CKD die of cardiovascular disease before reaching dialysis — statins, BP control, and antiplatelet therapy (when indicated) save more lives than dialysis access.
— Indicated when UACR ≥30 mg/g (especially ≥300) or HTN with CKD
— Lisinopril 10–40 mg, losartan 50–100 mg, valsartan 80–320 mg daily; titrate to maximally tolerated dose
— Do not combine ACEi + ARB (ONTARGET: harm, more AKI/hyperkalemia)
— Monitor: BMP at baseline, 2–4 weeks after initiation/titration, then periodically
— Acceptable: creatinine rise ≤30%, K ≤5.5
— Hold/reduce for K >5.5 despite diet/diuretic adjustment, creatinine rise >30%, symptomatic hypotension
— Cough → switch ACEi to ARB; angioedema → avoid both classes
— Dapagliflozin 10 mg or empagliflozin 10 mg daily
— Indicated if eGFR ≥20 and UACR ≥200 mg/g (DAPA-CKD, EMPA-KIDNEY)
— Reduces CKD progression, HF hospitalization, CV death
— Expect initial eGFR dip 3–5 mL/min (hemodynamic, reversible) — do not stop
— Hold for euglycemic DKA risk situations (prolonged fasting, surgery — hold 3–4 days preop)
— Counsel on genital mycotic infections, volume status
— Thiazide (chlorthalidone preferred, 12.5–25 mg) effective even at eGFR 30–45 (CLICK trial)
— Loop diuretic (furosemide, torsemide) when eGFR <30 or volume overload
— Amlodipine 5–10 mg — excellent add-on, no renal dose adjustment, well tolerated
— Especially useful in Black patients and isolated systolic HTN
— Finerenone (FIDELIO/FIGARO) in diabetic CKD with albuminuria; monitor K closely
Step 3 management: Build the regimen as ACEi/ARB + SGLT2i + thiazide or amlodipine, layered to target. Reassess BP and BMP every 2–4 weeks during titration, then every 3–6 months. Document each medication change with rationale — the CCS environment rewards stepwise titration over megadose monotherapy.
Board pearl: ACEi/ARB + SGLT2i is the modern renoprotective backbone — both reduce intraglomerular pressure and albuminuria via complementary mechanisms.
— BP above goal despite 3 agents at optimal doses including a diuretic, or controlled on ≥4 agents
— Confirm with ABPM (exclude white-coat), assess adherence (pharmacy refill data, witnessed dosing), screen secondary causes
— Spironolactone 12.5–25 mg daily (PATHWAY-2): superior to bisoprolol or doxazosin for resistant HTN
— Effective even when aldosterone is "normal"
— Monitor K weekly initially, especially with ACEi/ARB and eGFR <45
— Side effects: gynecomastia, mastodynia → switch to eplerenone if intolerable
— Beta-blockers (metoprolol succinate, bisoprolol, carvedilol) — preferred when concurrent CAD, HFrEF, AF; not first-line for HTN alone
— Hydralazine + isosorbide dinitrate — especially in Black patients with HFrEF or intolerance to RAAS blockade
— Clonidine, guanfacine — central sympatholytics; rebound HTN if stopped abruptly; reserved for refractory cases
— Minoxidil — last-line, requires loop diuretic + beta-blocker to manage fluid retention and reflex tachycardia
— NSAIDs — AKI, HTN, edema; counsel patients explicitly
— Metformin — hold at eGFR <30, caution 30–45
— Gadolinium-based contrast — minimize at eGFR <30
— Renally cleared drugs — dose-adjust gabapentin, allopurinol, digoxin, LMWH, DOACs per eGFR
— Bowel preps with phosphate — risk of phosphate nephropathy
— Dietary K restriction, loop or thiazide diuretic, correct acidosis (bicarb if HCO₃ <22)
— Patiromer or sodium zirconium cyclosilicate — enables continued ACEi/ARB/MRA dosing
CCS pearl: When a CCS case shows persistent BP elevation despite three agents, add spironolactone before chasing exotic diagnoses — but first verify adherence, check K, and screen for hyperaldosteronism with ARR (off MRA and amiloride for 4–6 weeks).
Step 3 management: Renal denervation is FDA-approved (2023) for refractory HTN — consider after lifestyle, adherence, and pharmacologic optimization fail.
— SPRINT-Senior subgroup: intensive control (<120) still benefited ambulatory adults ≥75 with CV mortality reduction
— Caveats: frail, institutionalized, multiple falls, orthostatic hypotension, dementia → target <130/80 or even <140/90
— Start low, go slow: initiate one agent at half dose, titrate every 4 weeks
— Prefer amlodipine, ARB, thiazide as first agents; avoid alpha-blockers as monotherapy (ALLHAT showed harm) and limit central sympatholytics (cognitive side effects)
— Deprescribe when symptomatic hypotension, falls, or eGFR drop disproportionate to expected
— Screen for polypharmacy, anticholinergic burden, and orthostatics at every visit
— Loop diuretics replace thiazides for volume (though chlorthalidone has data at lower eGFR)
— Spironolactone: caution; monitor K every 1–2 weeks initially
— SGLT2i can be initiated down to eGFR 20 and continued until dialysis
— ACEi/ARB: continue unless K uncontrolled or symptomatic hypotension; STOP-ACEi trial showed no benefit to routine withdrawal in advanced CKD
— Avoid NSAIDs, magnesium-containing laxatives, phosphate enemas
— Cirrhosis with HTN: avoid ACEi/ARB initially if MAP-dependent renal perfusion; nonselective beta-blockers serve dual role (portal HTN); use carvedilol or nadolol
— Spironolactone is first-line for ascites and helpful for BP
— Elderly CKD patients often have stiff vasculature + low intravascular volume — gentle diuretic titration, avoid aggressive sodium restriction below 1.5 g/day in frail elderly
Board pearl: In a frail 85-year-old with eGFR 28 and SBP 135 on three agents, the right answer is often to deintensify, not add a fourth drug. Falls and AKI are competing harms.
Step 3 management: Reassess BP targets annually as patients age — what was appropriate at 65 may cause falls at 82. Document goals-of-care conversations and individualized targets in the chart.
— Women with hypertensive nephrosclerosis are at high risk for superimposed preeclampsia, IUGR, preterm delivery, AKI
— Preconception counseling is critical: optimize BP, switch off teratogens, baseline creatinine and UACR
— Contraindicated: ACEi, ARBs, direct renin inhibitors, SGLT2i, MRAs, statins (relative)
— Preferred agents: labetalol, nifedipine ER, methyldopa, hydralazine
— BP target in pregnancy (CHAP trial, 2022): <140/90 improves outcomes vs. permissive management
— Low-dose aspirin 81–162 mg starting 12–28 weeks for preeclampsia prevention in CKD
— Co-manage with MFM and nephrology
— Primary HTN in adolescents is rising with obesity; nephrosclerosis is uncommon at pediatric ages
— Evaluate for secondary causes aggressively (renal artery stenosis, coarctation, renal parenchymal disease, endocrine)
— Use age/sex/height-percentile BP tables (AAP 2017)
— First-line: ACEi, ARB, CCB, thiazide; avoid ACEi/ARB in sexually active adolescent girls without reliable contraception
— Higher prevalence and earlier ESRD progression; APOL1 high-risk variants confer increased risk
— First-line: thiazide or CCB without proteinuria; add ACEi/ARB if UACR ≥30 mg/g or diabetes
— Greater BP response to diuretics/CCB than to monotherapy RAAS blockade — but combination overcomes this
— Address structural determinants (food access, medication cost, healthcare access)
— Calcineurin inhibitor (tacrolimus, cyclosporine)-induced HTN is common; CCB (amlodipine, isradipine) preferred — they also counter CNI vasoconstriction
Key distinction: Methyldopa is the historical gold-standard in pregnancy but labetalol and nifedipine ER are now first-line per ACOG due to better efficacy and tolerability.
Step 3 management: For any woman of reproductive age on ACEi/ARB, document contraception or counsel switch preconception. Missing this is a common malpractice and board pitfall.
— Hypertensive nephrosclerosis is the #2 cause of ESRD in the US
— Median time to ESRD varies: years to decades with optimized therapy; accelerated in Black patients, APOL1 high-risk, poor BP control
— Once eGFR <30, focus shifts to renal replacement preparation, transplant evaluation, vascular access planning
— LVH and HFpEF/HFrEF — leading cause of death
— Coronary artery disease, MI, stroke — risk multiplied by CKD
— Atrial fibrillation — CKD increases incidence and bleeding/stroke complexity
— Sudden cardiac death — disproportionate in dialysis patients
— Anemia of CKD — work up at eGFR <60 with Hb <10; iron studies first, then ESA if TSAT >20%, ferritin >100, and other causes excluded; target Hb 10–11.5 (avoid >11.5 per TREAT, CHOIR)
— CKD-MBD: monitor Ca, phos, PTH, vitamin D starting CKD stage 3b; phosphate binders if phos elevated; calcitriol or analogs for secondary hyperparathyroidism
— Metabolic acidosis: bicarbonate if HCO₃ <22 — slows CKD progression
— Hyperkalemia: as discussed
— Hyperuricemia/gout: allopurinol with renal dose adjustment
— Accelerated atherosclerosis with vascular calcification
— Erectile dysfunction — both vascular and pharmacologic (thiazides, beta-blockers); use PDE5 inhibitors safely with BP meds (avoid with nitrates)
— Cognitive decline — vascular dementia risk increases
— Uncommon but devastating: BP often >180/120, AKI, MAHA, encephalopathy, papilledema, pulmonary edema
— Requires ICU admission and parenteral therapy (see chunk 12)
Board pearl: Anemia, acidosis, and hyperparathyroidism appear at eGFR 45–60 — start labs (CBC, iron studies, PTH, 25-OH-D, BMP) at this threshold to avoid missing the silent progression.
Step 3 management: Build a CKD problem list that explicitly tracks each complication — board questions reward systematic surveillance over reactive management.
— SBP >180 or DBP >120 with acute target-organ damage: encephalopathy, ischemic/hemorrhagic stroke, acute MI, acute HF/pulmonary edema, aortic dissection, AKI, MAHA, eclampsia, retinopathy with papilledema
— Reduce MAP by ≤25% in the first hour, then to 160/100 over 2–6 hours, then normalize over 24–48 hours
— Exceptions (more aggressive):
— Nicardipine, clevidipine — titratable, avoid in HFrEF
— Labetalol — broad use, avoid in bradycardia/asthma/decompensated HF
— Nitroprusside — caution with renal/hepatic failure (cyanide toxicity)
— Esmolol — short half-life, ideal for dissection
— Hydralazine — pregnancy; unpredictable in others
— Do NOT rapidly lower in the ED — restart/optimize oral agents, arrange close outpatient follow-up within 24–72 hours
— Avoid PRN clonidine or short-acting nifedipine — overshoot and harm
— eGFR <30, rapid decline (>5 mL/min/yr), refractory hyperkalemia, refractory HTN, UACR >300, unclear etiology, suspected GN, biopsy consideration, dialysis access planning, transplant referral
— Refer for transplant evaluation at eGFR <20 (preemptive listing improves outcomes)
— AV fistula creation 6–12 months before anticipated dialysis
— Hypertensive emergency
— Acute uremic symptoms (pericarditis, encephalopathy)
— Severe hyperkalemia (>6.5 or ECG changes)
— Refractory volume overload
— New AKI superimposed on CKD requiring workup
CCS pearl: In a CCS hypertensive-emergency case, place arterial line, start IV nicardipine or labetalol, ICU admission, q15-min BP, target MAP reduction ≤25% first hour — then transition to oral agents and identify the trigger (nonadherence, drugs, secondary cause).
— #1 cause of ESRD; often coexists with HTN
— Long-standing DM (typically >10 yr type 1, variable type 2), retinopathy usually present (sensitive marker in type 1)
— Albuminuria precedes GFR decline; may have nephrotic-range proteinuria unlike nephrosclerosis
— Management overlap: ACEi/ARB, SGLT2i, finerenone, tight glycemic control (A1c ~7%)
— Active urinary sediment (dysmorphic RBCs, RBC casts), proteinuria often >1.5 g/day
— Systemic features depending on etiology (skin, joints, lungs)
— Requires serologies and often biopsy
— Treatment may include immunosuppression
— Family history (autosomal dominant), flank pain, hematuria, palpable kidneys, hepatic cysts, intracranial aneurysm risk
— Imaging diagnostic (multiple bilateral cysts, enlarged kidneys — opposite of nephrosclerosis)
— Tolvaptan slows progression in rapid progressors
— Childhood UTIs, scarring on imaging, asymmetric small kidneys
— Often with HTN that mimics nephrosclerosis
— Drug-induced (lithium, NSAIDs, aristolochic acid, Chinese herbs), heavy metals, autoimmune (Sjögren), sarcoid
— Bland sediment, low-grade proteinuria — overlaps with nephrosclerosis; medication history is key
— Atherosclerotic in elderly, fibromuscular dysplasia in young women
— Flash pulmonary edema, AKI on ACEi, asymmetric kidneys, abdominal bruit
— Confirm with duplex/CTA/MRA
— Revascularization rarely improves outcomes (CORAL); medical management preferred unless flash edema or refractory HTN
— Recent vascular procedure, livedo reticularis, eosinophilia, blue toes, low complements
Key distinction: Hypertensive nephrosclerosis has bland sediment, modest proteinuria (<1 g/day), bilateral small smooth kidneys, and proportionate clinical course. Deviations from this profile mandate alternative workup.
Board pearl: When DM and HTN coexist with retinopathy and modest proteinuria, diabetic nephropathy is the working diagnosis — but renoprotective therapy is identical (ACEi/ARB + SGLT2i + finerenone).
— Primary aldosteronism: hypokalemia, resistant HTN, incidental adrenal adenoma; ARR screening, confirmatory saline suppression, adrenal CT, AVS
— Renal artery stenosis: atherosclerotic or FMD; flash pulmonary edema, AKI on ACEi
— Pheochromocytoma: episodic spells, headache/palpitations/diaphoresis, orthostatic; plasma/urine metanephrines
— Cushing syndrome: central obesity, striae, hyperglycemia, hypokalemia; overnight DST, 24-hr urine cortisol, late-night salivary cortisol
— Hyperthyroidism: widened pulse pressure, tremor, weight loss; TSH
— Hyperparathyroidism: hypercalcemia, kidney stones, bone disease
— OSA: snoring, witnessed apneas, daytime somnolence, Epworth >10; PSG
— Coarctation of aorta: young patient, BP discrepancy upper/lower extremity, rib notching, radio-femoral delay
— Drug-induced: NSAIDs, oral contraceptives, decongestants, glucocorticoids, stimulants, cocaine, methamphetamine, licorice, erythropoietin, calcineurin inhibitors, VEGF inhibitors
— Multiple myeloma / amyloidosis — older patient, anemia, bone pain, hypercalcemia, proteinuria with low UACR but high UPCR (light-chain proteinuria dipstick-negative)
— Hepatorenal syndrome — in cirrhosis with ascites
— Cardiorenal syndrome — concomitant HF; volume management central
— Volume depletion / prerenal AKI — overdiuresis, GI losses
— Obstruction — BPH, stones, retroperitoneal fibrosis; renal US for hydronephrosis
— Contrast-associated AKI — recent imaging
— NSAID-induced AKI — common, reversible
Step 3 management: In a hypertensive patient with new "CKD progression," always check urine sediment, repeat creatinine after hydration, review medication list (especially NSAIDs and new ACEi/ARB titration), and obtain a renal US to exclude obstruction before attributing decline to nephrosclerosis.
Board pearl: Hypokalemia + HTN = think aldosteronism until proven otherwise — measure ARR before starting an MRA, which invalidates testing for 4–6 weeks.
— ACEi or ARB at maximally tolerated dose
— SGLT2 inhibitor if eGFR ≥20 and UACR ≥200, or diabetes, or HF
— Diuretic (thiazide or loop) tailored to eGFR and volume
— CCB (amlodipine) and/or MRA (spironolactone) for resistant HTN
— Statin — moderate-to-high intensity for all CKD patients age 50–75 (KDIGO, ACC/AHA); not initiated de novo in dialysis but continued if already on
— Aspirin — for established ASCVD; not routinely for primary prevention in CKD due to bleeding risk
— Bicarbonate for HCO₃ <22
— Iron, ESA if anemic per protocol
— Phosphate binder, vitamin D analog if CKD-MBD criteria met
— Sodium <2.3 g/day, DASH-style diet, plant-forward
— Protein moderation 0.6–0.8 g/kg/day in non-dialysis CKD (KDIGO/KDOQI), not severe restriction
— Avoid NSAIDs — give explicit written list of OTC products to avoid
— Tobacco cessation, alcohol moderation, weight loss
— Physical activity 150 min/week aerobic + resistance training
— Influenza annually
— Pneumococcal (PCV20 or PCV15+PPSV23)
— Hepatitis B — screen and vaccinate; higher dose schedule in CKD stage 4+ (prepare for dialysis)
— COVID-19 per current schedule
— RSV for adults ≥60
— Shingles at age ≥50
— After hospitalization, reconcile meds within 7 days
— BMP within 1–2 weeks post-discharge if RAAS or diuretic adjusted
— Nephrology follow-up within 2–4 weeks if eGFR <30 or new significant decline
Step 3 management: At every visit, address BP, CKD progression, ASCVD prevention, complications of CKD, and lifestyle — the "5-domain CKD visit." Document each.
Board pearl: Statin therapy in CKD is among the highest-yield interventions — don't withhold based on creatinine unless on dialysis without prior indication.
— Stage 1–2 (eGFR ≥60): annual if UACR <30; every 6 months if UACR 30–300
— Stage 3a (45–59): every 6 months
— Stage 3b (30–44): every 3–4 months
— Stage 4 (15–29): every 1–3 months, nephrology co-management
— Stage 5 (<15): monthly or more, RRT planning
— BMP, eGFR — track creatinine trajectory
— UACR — annually minimum, more often if titrating ACEi/ARB or SGLT2i
— CBC — annually; more often if anemic
— PTH, calcium, phosphate, 25-OH vitamin D — every 6–12 months once stage 3b+
— Lipid panel at diagnosis; recheck if changing therapy
— HbA1c if diabetic, every 3 months until at goal, then every 6
— Validated upper-arm device, twice daily for 7 days before each visit; discard day 1
— Target <125/75 home equivalent (≈ <130/80 office)
— Bring logs to every visit
— Medication adherence — single-pill combinations improve adherence (e.g., losartan/HCTZ, amlodipine/benazepril)
— Sick-day rules: hold ACEi/ARB, SGLT2i, diuretics, metformin, NSAIDs during acute illness with volume depletion (vomiting, diarrhea, sepsis) — "SADMANS" mnemonic — and resume when eating/drinking normally
— Pre-procedure: hold SGLT2i 3–4 days before surgery; communicate to surgical team
— Contrast counseling: discuss risks/benefits, hydration protocols
— Refer to renal dietitian at stage 3b
— Cardiac rehab if recent CV event
— Diabetes education if applicable
— Behavioral support for smoking cessation, weight loss
— Discuss dialysis vs. conservative management as eGFR approaches 20, especially in elderly/frail
— Code status, POLST, transplant candidacy
Step 3 management: Use structured visit templates to ensure each CKD visit covers BP, labs, meds, lifestyle, vaccinations, and advance care planning — board questions punish omissions.
Board pearl: Teach sick-day medication holding explicitly — it is a top cause of preventable AKI and a frequent Step 3 vignette.
— Intensive control (<120) reduces CV events but increases syncope, AKI, electrolyte abnormalities
— Document patient values, functional status, and informed agreement on target
— Reassess as the patient ages or develops frailty
— Discuss all modalities (in-center HD, home HD, peritoneal dialysis, preemptive transplant, conservative kidney management) as eGFR approaches 20
— Conservative management is a legitimate choice, especially in elderly/frail with limited expected survival benefit — Step 3 favors offering it explicitly
— Document capacity, surrogate decision-makers, and POLST/advance directives
— Hospital-to-home is a high-AKI window: RAAS blockade restarted without follow-up BMP, missed diuretic adjustments, NSAID restart
— Schedule BMP within 7–14 days after any med change
— Use medication reconciliation at every transition — admission, transfer, discharge
— Communicate eGFR-based dose adjustments to the patient and downstream providers
— Disparate burden of hypertensive nephrosclerosis in Black communities reflects structural inequities (food access, environmental stress, healthcare access, historical exclusion from trials)
— Screen for social determinants (medication cost, food security, housing, transportation) — assistance programs, 340B pharmacy, generic substitutions
— APOL1 testing: counsel about implications for prognosis and family screening; avoid stigmatization
— Driving safety in advanced CKD with cognitive impairment or syncope — state-specific reporting laws
— Workplace accommodations for dialysis schedules — ADA protections
— Avoid prescribing cascades (e.g., adding amlodipine for ankle edema instead of recognizing the cause)
— Polypharmacy review at every visit, especially in elderly
— Eligibility for renoprotective trials (e.g., novel agents in APOL1 nephropathy) — explain randomization, risks, voluntary participation
Step 3 management: When a frail 84-year-old with eGFR 14 and dementia approaches dialysis, a structured family meeting weighing conservative vs. dialytic care — with documented goals and surrogate input — is the correct answer, not reflexive AV fistula placement.
Board pearl: Always offer conservative kidney management as an explicit choice when survival benefit of dialysis is marginal.
— Hypertensive nephrosclerosis triad: LVH + hypertensive retinopathy + bilateral small kidneys with bland sediment and mild proteinuria
— SADMANS sick-day hold: Sulfonylureas, ACEi, Diuretics, Metformin, ARBs, NSAIDs, SGLT2i
— Resistant HTN add-on: "Spironolactone is the answer" (PATHWAY-2)
— SPRINT — intensive BP <120 reduces CV events and mortality in non-diabetic high-risk adults
— ACCORD-BP — in diabetics, intensive control reduced stroke but not composite CV
— CHAP — pregnancy BP <140/90 improves outcomes
— DAPA-CKD, EMPA-KIDNEY — SGLT2i renoprotection regardless of diabetes
— FIDELIO-DKD, FIGARO-DKD — finerenone in diabetic CKD
— CORAL — renal artery stenting no better than medical therapy
— STOP-ACEi — no benefit to routine ACEi withdrawal in advanced CKD
— CLICK — chlorthalidone effective at eGFR 15–30
— AASK — in Black patients with hypertensive nephrosclerosis, ACEi superior to amlodipine and metoprolol for slowing GFR decline when proteinuria present; lower BP target did not slow progression overall but benefited those with proteinuria
— Target BP <130/80 (KDIGO/ACC), aim <120 SBP if tolerated
— Acceptable creatinine rise after ACEi/ARB: ≤30%, recheck at 2–4 weeks
— Refer nephrology: eGFR <30, UACR >300, rapid decline
— Transplant referral: eGFR <20
— AV fistula: 6–12 months before anticipated dialysis
— Statin: all CKD patients age 50–75 not on dialysis
— APOL1 high-risk → accelerated nephrosclerosis/FSGS in African ancestry
— Hypokalemia + HTN → primary aldosteronism
— Flash pulmonary edema + AKI on ACEi → bilateral RAS
— Cocaine/meth → accelerated HTN and nephrosclerosis
— NSAIDs → reversible cause of CKD progression
— Resistant HTN → spironolactone, screen for aldosteronism and OSA
Board pearl: AASK established ACEi as preferred first-line in Black patients with hypertensive nephrosclerosis and proteinuria — overrides the general "thiazide/CCB first in Black patients without proteinuria" rule.
Step 3 management: Memorize the trial-to-management mapping — Step 3 stems frequently quote trial scenarios.
— 62-year-old Black man with 15-year HTN history, on lisinopril (often suboptimal dose), eGFR 48, UACR 180 mg/g, bland sediment, bilateral small kidneys on US, LVH on ECG
— Answer: hypertensive nephrosclerosis; intensify ACEi, add SGLT2i, target BP <130/80, statin
— Same patient but with dysmorphic RBCs and 2.5 g/day proteinuria → workup for GN, not nephrosclerosis
— Or with hypokalemia and resistant HTN → ARR for aldosteronism
— Creatinine rises from 1.3 to 1.5 after starting lisinopril → continue, recheck in 2 weeks (≤30% rise acceptable)
— Creatinine rises from 1.3 to 2.4 → stop, evaluate for bilateral RAS
— BP 156/92 on lisinopril, amlodipine, HCTZ at max doses → add spironolactone (confirm adherence, exclude white-coat first)
— CKD with UACR 250, eGFR 35, no diabetes → add dapagliflozin or empagliflozin
— 32-year-old on lisinopril plans pregnancy → switch to labetalol or nifedipine ER preconception; add aspirin 81 mg at 12 weeks
— SBP 220 with AKI and pulmonary edema → ICU, IV nicardipine or clevidipine, MAP reduction ≤25%/hr
— Aortic dissection → esmolol/labetalol first, target SBP <120 in 20 minutes
— K 5.7 on lisinopril → dietary K restriction, optimize diuretic, treat acidosis, consider patiromer rather than stopping the ACEi
— CKD patient with gastroenteritis arrives with AKI → held meds inappropriately resumed; reinforce SADMANS counseling
— 86-year-old, falls, SBP 122 on 4 agents → deintensify, target <140/90
— Discharge after MI, started on new ACEi → BMP in 7–14 days, follow-up clinic visit, med rec
Step 3 management: Read the age, comorbidities, eGFR trajectory, UACR, and BP control history in every stem — these determine whether to add, switch, hold, or deintensify.
Board pearl: When in doubt on Step 3, the answer is usually "optimize lifestyle + ACEi/ARB + SGLT2i + thiazide," with target <130/80 confirmed by HBPM.
Hypertensive nephrosclerosis is a slowly progressive, bland-sediment, low-proteinuria CKD diagnosed clinically in chronically hypertensive patients with bilateral small kidneys and end-organ damage — managed lifelong with a BP target <130/80 (ideally <120 systolic if tolerated), maximally titrated ACEi/ARB, SGLT2 inhibitor, diuretic, and aggressive ASCVD risk reduction.
— Long-standing HTN + LVH + hypertensive retinopathy + bilateral small smooth kidneys + UACR <300 + bland sediment
— Exclude diabetic nephropathy, glomerulonephritis, renovascular disease, secondary HTN, and obstruction before anchoring
— BP <130/80 with HBPM confirmation (intensify to <120 SBP per SPRINT when tolerated)
— ACEi or ARB at maximally tolerated dose; tolerate ≤30% creatinine rise; never combine ACEi + ARB
— SGLT2 inhibitor if eGFR ≥20 and UACR ≥200 or diabetes — modern renoprotective backbone
— Thiazide (chlorthalidone) or loop diuretic based on eGFR
— Spironolactone for resistant HTN (PATHWAY-2)
— Statin for all CKD age 50–75; lifestyle including sodium <2.3 g/day, DASH diet, protein 0.6–0.8 g/kg/day, exercise, smoking cessation, NSAID avoidance
— eGFR/UACR by KDIGO heat map; CBC, PTH, Ca, phosphate at stage 3b+
— Refer nephrology at eGFR <30, UACR >300, rapid decline; transplant at eGFR <20; AV fistula 6–12 months before dialysis
— Pregnancy: switch to labetalol/nifedipine/methyldopa, add ASA 81 mg
— Elderly/frail: individualize target, deprescribe to prevent falls
— Hypertensive emergency: ICU, IV agents, MAP reduction ≤25%/hour
— Sick days: SADMANS holds to prevent AKI
Board pearl: The single highest-yield intervention is sustained BP control plus RAAS + SGLT2i blockade — every other step orbits this core.
Step 3 management: Treat hypertensive nephrosclerosis as a longitudinal, multi-domain outpatient disease — BP, CKD progression, CV prevention, complications, lifestyle, and advance care planning revisited at every visit.