Lecture coverage map

Classify a patient as hypo-/eu-/hypervolemic from orthostatic vitals, JVP, mucosa/turgor, edema, lung exam, weight trend and urine output, and state which signs are unreliable (elderly turgor, beta-blockade)

Choose isotonic crystalloid (NS vs balanced) for volume resuscitation, know when hypotonic fluid is appropriate (free-water deficit only), and recognize hospital-acquired hyponatremia from hypotonic maintenance fluids and hyperchloremic acidosis from large-volume NS

Read a BMP in a fixed order (Na, K, Cl, HCO3, anion gap, BUN/Cr, glucose, then Ca/Mg/PO4), flag the values that are emergencies, and name the pattern (AGMA, NAGMA, alkalosis, prerenal) before the diagnosis

Exclude pseudo-/hypertonic hyponatremia (serum osm, glucose correction), then use urine osmolality (<100 = water excess, >100 = ADH active), urine Na (<30 vs >30) and volume exam to label hypovolemic, euvolemic or hypervolemic hyponatremia

Diagnose SIADH (euvolemic, UOsm >100, UNa >30, normal TSH and cortisol), name the common causes (SSRIs, carbamazepine, small-cell lung cancer, pneumonia, CNS disease, pain/nausea post-op), and start fluid restriction, stopping the offending drug; know salt tabs/urea are second line

Recognize beer potomania / tea-and-toast (dilute urine, poor solute intake, alcohol) and thiazide-induced hyponatremia (older women, low BMI, SSRI co-use, onset within weeks); stop the thiazide, feed solute, and anticipate rapid overcorrection once the water diuresis starts

Recognize edema + low urine Na as hypervolemic hyponatremia, treat the underlying disease with fluid restriction plus loop diuretic, avoid isotonic saline, and refer before any vaptan

Identify severe symptoms (seizure, coma, vomiting, obtundation), give 100–150 mL 3% NaCl over 10–20 min (repeat up to 3 times) targeting a 4–6 mEq/L rise per the ESE/ERA-EDTA 2014 guideline (Spasovski, PMID 24569496) and the SALSA trial (PMID 33104189), recheck Na every 2 h, and stop once symptoms resolve

State the 8 mEq/L per 24 h ceiling of the ESE/ERA-EDTA 2014 guideline (Spasovski, PMID 24569496) (4–6 in high risk: Na <115, alcohol use, malnutrition, hypokalemia, liver disease), recognize ODS (delayed dysarthria, dysphagia, quadriparesis 2–6 days after overcorrection), and know relowering with D5W ± desmopressin exists and is a nephrology call

Name the causes (no water access in the elderly/infant, GI and insensible loss, osmotic diuresis, DI), calculate free-water deficit, replace with oral water or D5W at ≤10–12 mEq/L per 24 h for chronic cases, and separate central from nephrogenic DI (lithium, hypercalcemia) by desmopressin response

Sort causes into GI loss (vomiting, diarrhea, laxatives), renal loss (loop/thiazide diuretics, hyperaldosteronism, RTA, hypomagnesemia) and shifts (insulin, beta-agonists, alkalosis); recognize U waves/QT prolongation; choose oral vs IV KCl, respect IV rates (10 mEq/h peripheral, 20 mEq/h monitored), target ≥4.0 in cardiac patients and replete Mg first

Grade severity, recognize the ECG progression (peaked T → PR/QRS widening → sine wave) and its unreliability, and suspect pseudohyperkalemia (hemolysis, fist clenching/tourniquet, marked thrombocytosis or leukocytosis) by repeating the draw without delaying treatment of a convincing emergency

Order, in sequence and in parallel where needed: IV calcium for ECG changes (stabilize), insulin + dextrose with serial glucose checks and nebulized albuterol (shift), then removal (loop diuretic if making urine, binder — sodium zirconium cyclosilicate or patiromer — and dialysis for refractory/anuric), and recheck K for rebound

Identify RAAS inhibitors, MRAs, K-sparing diuretics, TMP-SMX, NSAIDs, heparin, K supplements/salt substitutes and CKD or diabetic hypoaldosteronism (type 4 RTA: mild NAGMA + hyperK) as causes; decide what to stop or reduce, use low-K diet, loop diuretic, bicarbonate or a binder to keep RAAS blockade on board

Correct total Ca for albumin (or get ionized), order intact PTH first, then PTHrP, 25-OH D, 1,25-OH D, SPEP/UPEP and TSH as directed; place the result in the differential — primary HPT vs malignancy (PTHrP, osteolytic/myeloma, lymphoma), granulomatous disease, vitamin D or A excess, milk-alkali, immobilization, thiazides, lithium, hyperthyroidism, adrenal insufficiency, FHH

Treat severe or symptomatic hypercalcemia urgently with volume-assessed isotonic fluid, short-course calcitonin and prompt renal-informed antiresorptive treatment when indicated. Select IV bisphosphonate or denosumab with attention to etiology, kidney function and hypocalcemia risk; loop diuretics treat volume overload, not routine calcium clearance. Consider cause-specific glucocorticoids or dialysis in selected cases.

Interpret calcium with albumin, pH and clinical context; obtain ionized calcium when accuracy matters or corrected calcium is unreliable. Recognize symptomatic hypocalcemia and treat urgently; correct magnesium and the cause. Avoid routine calcium for asymptomatic TLS-associated hypocalcemia, while treating dangerous hyperkalemic ECG changes with IV calcium.

Suspect hypomagnesemia in long-term PPI use, loop/thiazide diuretics, alcohol use and diarrhea; recognize refractory hypokalemia or hypocalcemia as the clue; give IV MgSO4 for Mg <1.0, torsades or symptoms and oral otherwise; stop the PPI. Recognize hypermagnesemia in CKD patients on Mg laxatives/antacids (lost reflexes, hypotension, bradycardia) and treat by stopping the source, IV calcium, fluids/loop, dialysis if kidney failure

Name hypophosphatemia causes (refeeding, DKA treatment, alcohol use, respiratory alkalosis, phosphate binders/antacids, hyperparathyroidism) and replace IV when <1.0 mg/dL or symptomatic; name hyperphosphatemia causes (CKD, TLS, rhabdomyolysis) and the first steps (treat the cause, check calcium, diet, binders, dialysis when severe with hypocalcemia)

Read pH/PCO2/HCO3 to name the primary disorder, compute expected PCO2 = 1.5 × HCO3 + 8 ± 2 (Winter), apply the 0.7 rule for metabolic alkalosis and the acute/chronic 1 and 3.5 (resp acidosis) and 2 and 5 (resp alkalosis) rules, and call a second disorder when compensation is off

Calculate AG = Na − (Cl + HCO3), correct for albumin (2.5 per g/dL), run MUDPILES/GOLDMARK, check lactate, beta-hydroxybutyrate, osmolal gap (toxic alcohols) and salicylate level, and name the first-line treatment of each common cause (fluids/insulin for DKA, source control for sepsis, fomepizole/dialysis for toxic alcohol)

Compute ΔAG/ΔHCO3 and read <1 as an added NAGMA, 1–2 as pure AGMA, >2 as an added metabolic alkalosis; recognize the common mixed pictures (DKA + vomiting, sepsis + respiratory alkalosis, COPD + diuretic alkalosis)

Recognize non-anion-gap acidosis; use urine Na+K−Cl as a context-dependent indirect ammonium clue. A negative value can support GI bicarbonate loss; a positive value is not diagnostic of RTA and may be misleading with low urine sodium or unmeasured urinary anions. Proximal RTA may have a negative gap after bicarbonate depletion. Treat the cause and individualize alkali.

Fill a one-row-per-type table: defect, urine pH, serum K, classic causes (type 1: Sjögren, amphotericin, lithium; type 2: Fanconi, myeloma, tenofovir, acetazolamide; type 4: diabetes, hypoaldosteronism, ACEi/NSAID/heparin/TMP-SMX), stones/nephrocalcinosis in type 1, and treatment (alkali; fludrocortisone or loop for type 4)

Recognize HCO3 >28 with hypokalemia, use urine chloride (<20 saline-responsive: vomiting, NG suction, diuretics, contraction, post-hypercapnia; >20 resistant: hyperaldosteronism, Bartter/Gitelman, licorice), treat with isotonic saline + KCl, stop the diuretic or purging and add a PPI/antiemetic, and expect PCO2 to rise 0.7 per mEq HCO3

Suspect EDKA in an SGLT2i user with malaise, nausea or dyspnea and an AG acidosis despite glucose <250, confirm with beta-hydroxybutyrate, hold the drug 3–4 days before surgery and on sick days, and treat with insulin plus dextrose

Predict and monitor the electrolyte effects of loops (hypoK, hypoMg, hypoCa, alkalosis), thiazides (hypoNa, hypoK, hyperCa, hyperuricemia), K-sparing/MRAs (hyperK), acetazolamide (NAGMA), and order a BMP 1–2 weeks after starting or changing a diuretic, especially in the elderly and with RAAS blockade

State the KDIGO 2024 definition (>3 mo of GFR <60 or a marker of damage), distinguish CKD from AKI/AKD, and frame CKD as cause–GFR–albuminuria

Place a patient in the KDIGO 2024 G1–G5 × A1–A3 grid and translate the color to monitoring frequency and referral urgency

Order spot UACR for albuminuria, explain why dipstick misses A2, know false-positive causes, and confirm with a repeat before acting

Name the race-free CKD-EPI 2021 inputs, list when creatinine misleads (muscle mass, drugs, non-steady state), and know cystatin C as the confirm test

Rank DM, HTN, GN, PKD as causes; take the history, order UA with microscopy, UACR and renal US; recognize GN red flags (RBC casts, heavy proteinuria) that need referral

Screen T2D annually with UACR + eGFR, recognize typical DKD, and flag atypical features (no retinopathy, hematuria, rapid fall)

Explain why "hypertensive CKD" is over-called, name the features that fit (long HTN, bland UA, low proteinuria) and those that do not

Suspect ADPKD from family history/flank pain/HTN, confirm with ultrasound, counsel on BP, cyst complications and aneurysm-screening indications, refer; know tolvaptan exists but is specialist-prescribed

Compute eGFR slope, name albuminuria as the main driver, and read a KFRE 2-/5-year % against the KDIGO 2024 risk thresholds (refer at >3–5%/5 yr; plan access/modality at >40%/2 yr)

State the KDIGO 2021 BP target with standardized measurement, teach home BP, choose ACEi/ARB first when albuminuric, add CCB/thiazide, and never combine ACEi+ARB

Check Cr/K at 1–2 wk, accept a ≤30% Cr rise, act on >30% or K >5.5 (KDIGO 2024 practice point), and list the hold triggers (acute illness, contrast, hypotension, pregnancy, angioedema)

Prescribe for albuminuric CKD down to eGFR 20 with or without diabetes (KDIGO 2024), expect and explain the initial eGFR dip, counsel on GU infection/volume/euDKA, hold on sick days

Identify appropriate add-on therapy in T2D with CKD: finerenone with persistent albuminuria despite tolerated RAS blockade, eGFR ≥25 and acceptable potassium; trial entry K ≤4.8 differs from US initiation limit ≤5.0 with monitoring. Select GLP-1 RA for indicated metabolic, cardiovascular and kidney benefit; monitor tolerability and avoid unsupported fixed sequencing.

Screen Hgb by stage, order ferritin/TSAT and rule out other causes first, replete iron before ESA, state the KDIGO 2026 ESA Hgb ceiling (<11.5) and why (stroke/thrombosis)

Know when to check Ca/PO4/PTH/25-OH D by stage, counsel dietary phosphorus first, name binder classes, replete nutritional vitamin D, and leave active D/calcimimetics to nephrology

Evaluate persistent metabolic acidosis and consider dietary or pharmacologic treatment to prevent clinically consequential acidosis, with KDIGO2024 giving bicarbonate <18 mmol/L as an example. Treatment at19–21 is individualized rather than automatic; monitor BP, potassium, sodium load and volume.

Counsel diet/salt substitutes, review culprit drugs (NSAIDs, TMP, K-sparing), use loop diuretic or a binder (patiromer/SZC) to keep RAASi, know when to hold RAASi, and treat acute hyperkalemia per protocol

Use the label's kidney-function measure, choose dose-reduction vs interval-extension, and adjust the common offenders (antibiotics, DOACs, gabapentinoids, metformin thresholds, insulin/sulfonylureas)

Stop NSAIDs ("triple whammy"), apply contrast and gadolinium precautions, flag lithium, phosphate bowel preps, aminoglycosides and long-term PPIs, and offer analgesic alternatives

Recite SADMANS, say what not to hold (statins, beta-blockers, steroids, transplant drugs), and tell a patient when to stop and restart

Apply the KDIGO 2024 referral triggers (G4, A3, eGFR fall >5/yr, resistant HTN, persistent K or hematuria, unclear cause, KFRE >3–5%/5 yr) and send the right data

Start education at G4 (or 2-yr KFRE >40%, KDIGO 2024), compare in-center HD, home HD, PD, transplant and conservative care in plain terms, and explain that start is symptom-driven (IDEAL trial, per 02-Medical-Education/Student-References/dialysis-initiation-student-handout)

Order AVF > AVG > catheter, protect the non-dominant arm (no PICC, IV or BP cuff) from G4 onward, know maturation time, and recognize access infection

Refer for pre-emptive transplant evaluation at G4/eGFR approximately 20 (KDIGO 2024), name the common contraindications, raise living donation, and describe conservative care as active symptom-focused management

Recognize uremia (anorexia, nausea, pruritus, confusion, rub, bleeding), recite AEIOU, and call nephrology the same day

Treat CKD as an ASCVD risk enhancer, start a statin in most adults ≥50 with CKD (KDIGO 2013 lipid guideline), and avoid "renalism" (withholding proven cardiac therapy)

Give the plain-language counsel: sodium <2 g and protein approximately 0.8 g/kg (KDIGO 2024; no very-low-protein diets outside specialist care), phosphorus additives, individualized potassium, smoking, weight

Read SG, pH, protein, blood, LE/nitrite, glucose, ketones; name false +/− traps (concentrated or alkaline urine → false + protein; dilute urine, light chains, myoglobin → false −; heme + with no RBCs = hemoglobin or myoglobin)

Match cast to setting (RBC → GN; WBC → pyelo/AIN; muddy-brown granular → ATN; fatty/oval fat bodies → nephrotic; waxy → chronic; hyaline → nonspecific); judge contamination by squamous cells; recognize common crystals

State that ≥5% acanthocytes (threshold per glomerular-vs-urologic-hematuria-review) or RBC casts point to a glomerular source, that absence does not exclude GN, and that it needs fresh urine and an experienced reader

Choose first-morning UACR for albumin screening and appropriate UPCR or timed protein quantification for suspected non-albumin or heavy proteinuria; classify A1 <30, A2 30–300 and A3 >300 mg/g. Distinguish albuminuria categories from total protein and nephrotic-range protein excretion.

Recognize benign proteinuria (fever, exercise, orthostatic in tall teens/young adults); confirm with repeat first-morning sample or split day/night collection; reassure without further workup when orthostatic

Define microhematuria (≥3 RBC/hpf by microscopy, not dipstick alone); route by sediment + proteinuria (dysmorphic/casts/protein → nephrology; isomorphic, no protein → AUA/SUFU risk-tiered CT urography ± cystoscopy); never attribute hematuria to anticoagulants or UTI without confirming it resolves

Recognize nephrotic and nephritic patterns and build an age-appropriate differential; nephritic disease may have nephrotic-range proteinuria, and sediment/albumin findings do not alone establish the histologic diagnosis.

Recognize the typical childhood nephrotic presentation in which empiric glucocorticoids without routine biopsy are appropriate; atypical, syndromic or steroid-resistant presentations need a different specialist evaluation. A clinical steroid-sensitive phenotype is not histologic proof of MCD.

Suspect FSGS in an adult (esp. Black patient) with nephrotic syndrome ± HTN/CKD; list secondary causes (obesity, HIV, reflux/low nephron mass, heroin, pamidronate, sickle cell) that change management (treat cause, no steroids); know diagnosis is by biopsy

Suspect MN in an adult >40 with nephrotic syndrome; order anti-PLA2R; screen for secondary causes (age-appropriate cancer screening, HBV/HCV, SLE, NSAIDs/penicillamine); know renal vein thrombosis risk

Screen diabetes with UACR and eGFR; recognize albuminuric and nonalbuminuric DKD. Identify active sediment, rapid decline, atypical timing or systemic findings that warrant evaluation for another or additional cause; biopsy is individualized.

Recognize synpharyngitic gross hematuria or persistent microhematuria ± proteinuria in a teen/young adult with normal complement; know diagnosis is by biopsy; name supportive care (BP, ACEi/ARB, SGLT2i) and refer; recognize the HSP tetrad (purpura, arthralgia, abdominal pain, nephritis) in a child

Recognize nephritic syndrome 1–3 wk after pharyngitis and 3–6 wk after impetigo in a child; order ASO/anti-DNase B and C3/C4 (low C3, normal C4); manage supportively (salt/fluid restriction, loop diuretic, BP control); know C3 should normalize by 8–12 wk

Screen every SLE patient with UA + UPCR + Cr at diagnosis and each visit; recognize active sediment/proteinuria/rising Cr as LN; order ANA, anti-dsDNA, C3/C4 (both low); refer urgently for biopsy; know class drives therapy (steroids + MMF or cyclophosphamide — names only)

Recognize RPGN (Cr rising over days–weeks + active sediment ± systemic or pulmonary symptoms); send the stat panel (ANCA PR3/MPO, anti-GBM, ANA/dsDNA, C3/C4, CXR, renal US); call nephrology the same day; do not wait for biopsy; pair c-ANCA/PR3 with GPA and p-ANCA/MPO with MPA

Recognize hemoptysis + AKI + hematuria as pulmonary-renal syndrome; send anti-GBM with ANCA; know it is the GN where plasmapheresis is urgent and nephrology is called immediately

Order and read the first-line GN panel: C3/C4 pattern (both low → SLE, cryo, endocarditis, MPGN; low C3 normal C4 → PIGN, C3G; normal → IgAN, ANCA, anti-GBM, MCD/FSGS/MN), ANA/anti-dsDNA, ANCA, anti-GBM, anti-PLA2R, HBV/HCV/HIV, SPEP/FLC (>50 y), blood cultures if febrile

In every adult with new nephrotic syndrome check glucose/A1c, HIV, HBV/HCV, syphilis, ANA, SPEP/UPEP/FLC (esp. >50 y or dipstick-negative proteinuria), review drugs (NSAIDs, lithium, pamidronate, interferon), do age-appropriate cancer screening

Anticipate thromboembolism (RVT, DVT/PE; highest in MN, albumin <2–2.5), infection (encapsulated organisms, pneumococcal vaccine, peritonitis in children), AKI (over-diuresis, RVT), hyperlipidemia (statin), protein malnutrition; know anticoagulation is a weighed decision made with nephrology

Explain Starling forces (underfill vs overfill); separate nephrotic edema (periorbital, low albumin, normal JVP, proteinuria) from cardiac (JVD, S3, BNP) and hepatic (ascites, stigmata) using UA, albumin, BNP, echo

Manage nephrotic edema with sodium restriction and monitored loop diuresis; assess response and volume, consider sequential nephron blockade when resistant, and reserve IV albumin for selected refractory circumstances with specialist input. Monitor BP, weight, kidney function and electrolytes.

Start/titrate ACEi or ARB (accept ≤30% Cr rise per KDIGO 2024; recheck K/Cr in 1–2 wk), add SGLT2i when eGFR allows, target BP <130/80, statin for nephrotic lipids, sodium restriction; know sick-day holds

Refer: nephrotic syndrome in any adult, hematuria + proteinuria, active sediment, suspected RPGN (same day), unexplained AKI, SLE with renal signs, DKD with atypical features. Know biopsy contraindications (uncontrolled BP, bleeding/anticoagulation, small or solitary kidney) and that typical childhood MCD, classic PSGN and classic DKD are usually not biopsied

Link NSAIDs → MCD/MN (and AIN), lithium → FSGS/MCD, pamidronate → collapsing FSGS, hydralazine/PTU/levamisole-cocaine → ANCA vasculitis, interferon/anabolic steroids → podocytopathy; stop the drug; avoid NSAIDs in any proteinuric patient

Pair HBV → MN, HCV → MPGN/cryoglobulinemic GN (low C4, RF+), HIV → HIVAN (collapsing FSGS, large echogenic kidneys); know antiviral therapy is first-line, so viral serologies belong in every GN workup

Consider collagen-IV-related disease with persistent familial hematuria; assess hearing, ocular findings, albuminuria, BP and kidney-function trajectory. A thin basement membrane pattern is not a guarantee of a lifelong benign course; refer for genetic and nephrology assessment.

State the creatinine (≥0.3 mg/dL in 48 h or ≥1.5× in 7 d) and urine-output criteria and stage 1–3 a given patient

Ignore the printed eGFR when creatinine is moving, follow the creatinine trend, and explain the nephrectomy example

Sort an AKI into the three compartments from history, exam, BMP, UA and bladder/renal US; name the first test for each

Identify volume-depletion AKI (losses, orthostasis, BUN:Cr, low FENa), give isotonic crystalloid with reassessment, stop the hold-list drugs

Calculate FENa, apply the <1% / >2% cut-offs (BMP guide Part 4) only to the oliguric prerenal-vs-ATN question, and list the confounders (diuretics, CKD, sepsis, contrast, obstruction)

Map muddy brown casts → ATN, WBC casts/sterile pyuria → AIN, RBC casts/dysmorphic RBCs → GN (urgent), hyaline → prerenal; know urine eosinophils are not useful

Order renal + bladder US for any unexplained AKI, read hydronephrosis grade and post-void residual, know when non-contrast CT is next and that a negative US does not exclude obstruction

Recognize ATN after shock/sepsis/surgery, describe initiation–maintenance–recovery, give supportive care, explain why loop diuretics do not treat ATN

Recognize non-oliguric AKI 5–7 days into gentamicin or vancomycin, name the amplifiers (duration, volume depletion, combined nephrotoxins), stop/substitute, check levels, use extended-interval dosing

Distinguish contrast-associated and contrast-induced AKI, recognize high-risk situations and choose risk- and volume-informed prophylaxis. Isotonic bicarbonate is an alternative with no demonstrated advantage over saline, not an ineffective fluid. Do not use NAC or prophylactic dialysis routinely; handle metformin by the named policy.

Suspect from trigger + myalgia + dark urine, confirm with CK (>1,000 U/L; risk rises with CK), read heme-positive/RBC-negative dipstick, start goal-directed crystalloid, watch K+/Ca/phos and compartment syndrome

Suspect AIN from drug timeline (beta-lactams/sulfa/FQ in weeks, PPIs in months, NSAIDs) plus sterile pyuria/WBC casts, know the triad is usually absent, stop the drug, refer if creatinine does not fall

Explain afferent (NSAID) + efferent (ACEi/ARB) + volume (diuretic) physiology, spot the combination on a med list, hold the NSAID first

Recognize the expected early hemodynamic change after ACEi/ARB or SGLT2i initiation without equating the two drug classes. Recheck BP, creatinine and potassium after RAASi initiation or dose increase (usually within 2–4 weeks, earlier when clinically needed); evaluate a rise over 30% within 4 weeks or any clinical concern for AKI, volume depletion or hyperkalemia. An initial reversible SGLT2i eGFR dip alone is generally not a reason to stop it.

Make an individualized temporary-hold and restart plan during dehydrating illness or reduced intake, with particular attention to SGLT2i, metformin, diuretics and RAAS inhibitors; avoid NSAIDs and reconcile medication exposure in every AKI. Fever alone is not a universal hold instruction.

Name the culprits (IV acyclovir, high-dose methotrexate, TMP-SMX, uric acid/TLS, ethylene glycol), recognize crystals + AKI after a high-dose IV drug in a dry patient, prevent/treat with hydration and drug stop

Suspect obstruction (BPH, anuria or alternating output, palpable bladder, solitary kidney, stone pain), get bladder scan/US, place a Foley or call urology, know obstruction can exist without hydronephrosis

Recognize post-obstructive diuresis, monitor urine output, BP, weight and electrolytes closely, and individualize partial fluid replacement and composition to volume and sodium rather than matching every milliliter automatically.

Read a creatinine rise in decompensated HF as congestion not depletion; continue or escalate diuresis, withhold fluids, know when to refer

Recognize HRS-AKI in cirrhosis with ascites after prompt assessment and correction of hypovolemia when present; evaluate alternative causes and mixed injury. Do not require an automatic48-hour albumin challenge or absolute absence of proteinuria/tubular injury. Refer promptly for volume-assessed albumin/vasoconstrictor treatment and transplant evaluation.

Identify high-risk patients (bulky high-grade lymphoma/leukemia starting therapy), recognize the big-four labs with AKI, treat hyperkalemia first, know allopurinol vs rasburicase + IV fluids for prevention

Recite AEIOU with thresholds and recognize them at the bedside; call nephrology early for unexplained AKI, no improvement at 48–72 h, glomerular sediment, refractory K+ or acidosis

Decide give vs stop by repeated volume/perfusion exam, prefer balanced crystalloid (saline for contrast prophylaxis), do not chase oliguria with fluid, no renal-dose dopamine, no loop diuretic to "treat" AKI

Recognize ECG changes, sequence calcium → insulin/glucose → removal, and connect refractory K+, acidosis, pulmonary edema and uremia to the AEIOU decision

Renally dose or hold narrow-margin and renally cleared drugs (aminoglycosides, vancomycin, metformin and others) from the creatinine trend not the eGFR, and recheck as function changes

Document the AKI episode at discharge, arrange follow-up with creatinine, BP, volume, med-rec and albuminuria by 3 months, restart held RASi/SGLT2i deliberately, label persistent loss as AKD/CKD

For an unexpected creatinine rise in clinic: repeat BMP, review meds and intake, UA, bladder scan; choose same-day ED vs 48–72 h recheck from K+, symptoms, output and trajectory

Perform or coach a guideline-compliant reading (5-min seated rest, correct cuff size, arm at heart level, empty bladder, 2–3 readings averaged) and name the errors that falsely raise BP

Prescribe the 7-day HBPM protocol (AM+PM duplicates, discard day 1, average ≥130/80 = HTN), read ABPM thresholds (24-h ≥130/80, day ≥135/85, night ≥120/70), and classify white-coat vs masked vs sustained HTN

Stage BP (normal / elevated / stage 1 / stage 2) and decide drug-first vs 3–6 mo lifestyle-first using stage 1 + PREVENT ≥7.5% or stage 2 (AHA/ACC 2025)

State <130/80 for most adults incl. diabetes and CKD; adjust for frail older adults; check standing BP and manage orthostatic hypotension without abandoning treatment

Counsel on weight loss, DASH-style eating, sodium reduction, physical activity and alcohol moderation using population-average BP estimates. Individualize potassium-enriched foods or salt substitutes to current potassium, kidney function and medications; eGFR alone does not establish safety.

Name the four first-line classes (thiazide-type, DHP-CCB, ACEi, ARB), prefer chlorthalidone/indapamide over HCTZ, start two agents for stage 2 (single-pill), and recheck Na/K 4–12 wk (thiazide hyponatremia/hypokalemia, gout)

Match agent to comorbidity: ACEi/ARB for albuminuria, diabetes, CKD, HFrEF, post-MI; CCB/thiazide add-ons; beta-blocker only with a compelling indication; never ACEi + ARB; no ACEi/ARB in pregnancy

Counsel on cough (switch to ARB), angioedema (stop, never rechallenge ACEi), hyperkalemia; list contraindications (bilateral RAS, pregnancy, K >5.0) and the BMP recheck at 1–2 wk

Interpret a ≤30% creatinine rise (RAASi; Bakris & Weir, PMID 10724055) or a 3–5 mL/min eGFR dip (SGLT2i) in the first 1–4 wk as expected and continue (recheck 2–4 wk, KDIGO 2024); hold and look for volume depletion, NSAIDs, or RAS if >30% and rising, K ≥5.5, or hypotension

Define it (above goal on 3 drugs incl. a diuretic, or controlled on ≥4), exclude pseudoresistance (technique, adherence, white coat via HBPM/ABPM), screen secondary causes, and add spironolactone 4th-line (eGFR ≥45, K checks)

List the red flags (onset <30 or >50, resistant, hypokalemia, bruit, flash pulmonary edema, paroxysms, young woman) and order an aldosterone-renin ratio, knowing which drugs confound it and that universal screening in resistant HTN is Class 1

Distinguish FMD (young woman, "string of beads") from atherosclerotic RAS (older, vascular disease, AKI on ACEi, flash pulmonary edema, asymmetric kidneys); order duplex, CTA or MRA by eGFR; know medical therapy is first-line and revascularization is for FMD, flash edema, or declining GFR

Recognize paroxysmal headache / palpitations / sweating with labile HTN and order metanephrines (plasma free, or urine 24-h collection; mind interfering drugs/foods); refer before any procedure (alpha-blockade first)

Screen OSA with STOP-BANG and take a medication/substance history (NSAIDs, decongestants, OCPs, steroids, stimulants and atomoxetine, licorice, alcohol, energy drinks) before adding a fourth drug

Triage BP ≥180/120 by acute end-organ damage (encephalopathy, stroke, ACS, dissection, pulmonary edema, AKI, eclampsia); treat emergency with IV nicardipine/labetalol, lower MAP 10–25% in hour 1 (AHA/ACC 2025) with condition-specific exceptions; treat asymptomatic severe HTN orally with 1–2 wk follow-up, no IV

Recognize the phenotype (long-standing HTN, slow eGFR decline, bland UA, low-grade proteinuria), know HTN is listed as the #2 cause of ESKD, and name findings that should prompt another diagnosis (heavy proteinuria, hematuria, rapid decline) and the management (BP control, RAASi, SGLT2i)

Use age/sex/height percentile tables for <13 y and static adult cutoffs for ≥13 y (120/80, 130/80, 140/90); measure arm and leg BP for coarctation; know children <6 y or with diastolic-predominant HTN need a secondary workup (renal parenchymal/renovascular first)

Define preeclampsia (new HTN ≥140/90 + proteinuria or organ dysfunction after 20 wk; severe ≥160/110, headache, RUQ pain, HELLP labs); treat chronic HTN ≥140/90 (CHAP); treat ≥160/110 within 30–60 min with IV labetalol, IV hydralazine or PO nifedipine; avoid ACEi/ARB/atenolol; know delivery is definitive and MgSO4 prevents seizures

Classify a case as CRS type 1–5 (acute/chronic, heart→kidney vs kidney→heart, systemic) and explain that venous congestion, not low output, is the usual driver of kidney dysfunction in acute HF

Dose above the threshold (IV in decompensation; higher dose with lower eGFR; furosemide PO bioavailability is unreliable), double the dose if no response, and judge response at about 2 h by urine output and spot urine Na (<50–70 mmol/L = inadequate)

Assess diuretic resistance, sodium intake, adherence, absorption, volume and kidney function; optimize loop therapy and consider sequential nephron blockade with close monitoring. MRA and acetazolamide are context-dependent options, not mandatory steps in a universal fixed ladder.

Name the four pillars (ARNI or ACEi/ARB; carvedilol, metoprolol succinate or bisoprolol; MRA; SGLT2i), state that all four are started early at tolerated doses rather than maximizing one first, and name the monitoring labs (BMP, K)

Apply the eGFR/K rules: SGLT2i start at eGFR ≥20 and, once started, continue below 20 until dialysis unless not tolerated (KDIGO 2024; corrected 2026-10-12 — the earlier "continue down to 20" was wrong); steroidal MRA needs eGFR >30 and K <5.0; ARNI needs a 36-h ACEi washout; ACEi/ARB are continued in advanced CKD with monitoring; never stop GDMT for a modest creatinine rise

State who qualifies (T2D + CKD with persistent albuminuria on a tolerated ACEi/ARB, eGFR ≥25, K ≤5.0; separately HF with LVEF ≥40%, FINEARTS-HF PMID 39225278), the starting dose by eGFR (10 vs 20 mg), and the 4-wk K/eGFR check; do not combine with spironolactone

Give individualized temporary medication holds during significant volume-depleting illness, with explicit restart and monitoring instructions. Review SGLT2 inhibitors, metformin, diuretics and RAS-active agents by indication, intake, volume, kidney function and potassium; do not prescribe a universal restart order.

Recognize HRS-AKI in cirrhosis with ascites, assess competing and overlapping causes and response to resuscitation when indicated, and obtain hepatology/nephrology input. Avoid automatic prolonged albumin in a euvolemic or overloaded patient; vasoconstrictor and albumin therapy require specialist and volume assessment.

Place a patient in CKM stage 0–4 from adiposity, metabolic risk factors, CKD (albuminuria does the staging work), subclinical vs clinical CVD; use it to explain why BP, glucose, lipids and kidney protection are treated as one problem

Recognize colic ± hematuria; order non-contrast CT first-line, renal US in pregnancy/young/recurrent; read "stone + hydro"

Give NSAID-first analgesia, offer α-blocker MET for 5–10 mm distal stones, and name the drainage emergencies (fever/infected obstruction, AKI, solitary kidney, intractable pain)

Match CaOx/CaP/uric acid/struvite/cystine to risk factors; prescribe fluids ≥2.5 L, low Na, normal Ca, thiazide/citrate/allopurinol by indication; send recurrent/high-risk formers for 24-h urine

Decide when to culture, treat ASB only in pregnancy/pre-procedure, apply the "chronic catheter = 100% bacteriuric" rule (IDSA 2019), not treat delirium + bacteriuria alone; name recurrent-UTI prevention and urology red flags

Recognize pyelo (fever, CVA tenderness, WBC casts), choose outpatient vs admit, dose antibiotics by eGFR (avoid nitrofurantoin at low eGFR — fosfomycin or cephalexin instead), and image when not improving at 48–72 h, male, stones, CKD, or suspected obstruction

Spot the palpable bladder + rising creatinine, check PVR, place a Foley, recheck BMP, and start α-blocker ± 5-ARI with urology follow-up

Explain why creatinine rises only with bilateral or solitary-kidney obstruction, order renal US first, treat fever + obstruction as an emergency, and know stent vs nephrostomy as the urology/IR options

Define POD (>200 mL/h after relieving bilateral/solitary obstruction), monitor UOP and lytes q4–12 h, replace about half the output with half-normal saline, and avoid chasing physiologic diuresis

Take the family history, apply age-based US cyst criteria, explain 50% transmission (handout §5), and advise at-risk relatives when (≥18, repeat if negative) and whether to screen, including genetic testing when imaging is equivocal

Control BP with ACEi/ARB, recognize cyst hemorrhage vs infection vs stone, know liver cysts are common, screen for ICA only with family history/high-risk job, and state that tolvaptan is a nephrology-prescribed option for rapid progressors needing LFT monitoring

Flag hematuria + hearing loss + family history as Alport, call isolated familial microhematuria with normal function TBMN, and recognize bland-urine familial CKD as ADTKD; refer rather than work up

Reassure on a thin-walled anechoic cyst (I/II: no follow-up), know IIF means surveillance imaging, and send III/IV to urology; explain why a 25-year-old with bilateral cysts is a different question

Order multiphasic CT or MRI for an enhancing solid mass and refer to urology; name the red flags (hematuria, flank pain, mass, weight loss, smoking, paraneoplastic features) and recognize fat-containing AML as benign

Pick US for hydronephrosis/screening, non-contrast CT for stones, multiphasic CT/MRI for masses, duplex or CTA/MRA for RAS, MAG3 renogram for obstruction-vs-not; say when no imaging is needed

Distinguish contrast-associated from contrast-induced AKI and IV from relevant arterial procedures. In AKI or eGFR <30, weigh need, alternatives and volume-safe isotonic prophylaxis; do not reflexively cancel necessary imaging. Apply the explicitly named metformin policy and choose a Group II GBCA when an indicated enhanced MRI is needed, using a diagnostic dose.

Suspect RAS with resistant HTN, flash pulmonary edema, AKI after ACEi/ARB, bruit, or a young woman (FMD); screen with duplex, confirm with CTA/MRA; treat medically first and know stenting helps few (ASTRAL/CORAL)

Read a pregnancy creatinine (>0.8–0.9 is abnormal), expect physiologic right hydronephrosis, screen and treat ASB, admit pyelonephritis, define preeclampsia (≥20 wk HTN + proteinuria/organ injury), stop ACEi/ARB, use labetalol/nifedipine, avoid NSAIDs

Choose the right kidney-function estimate for a label, keep loading doses and reduce maintenance, and name the common renally cleared drugs needing adjustment (gabapentin, DOACs, antibiotics, opioids — avoid morphine/meperidine)

Review nephrotoxic and hemodynamically active medicines, recognize high-risk combinations, and give individualized temporary-hold and restart instructions during significant dehydration or acute illness. A mild fever alone is not a universal hold trigger. Coordinate transplant medication changes with the transplant team.

Explain hemodynamic AKI, AIN, and CKD risk; identify who must not take them (CKD 3b+, HF, diuretics + RAAS blockade, elderly, volume-depleted); offer acetaminophen/topical alternatives

Recognize aminoglycoside/vancomycin kidney toxicity and assess duration, exposure, volume and co-nephrotoxins. Use indication- and kidney-function-specific dosing with drug monitoring; extended-interval aminoglycosides are not universal for synergy, unstable AKI or dialysis. Use AUC-guided vancomycin monitoring when indicated and reassess the antibiotic plan if injury occurs.

Recognize early NDI (polyuria, low urine osm) vs late CKD, check levels, know NSAIDs/ACEi/thiazides raise lithium, and coordinate with psychiatry before changing anything

For US labeling, avoid starting metformin at eGFR 30–44, reassess continuation below45 and stop below30; ADA–KDIGO recommends 1,000 mg/day at30–44 when continued. Hold during significant acute illness/AKI. For IV iodinated contrast under ACR policy, continue if stable eGFR ≥30 with no AKI; hold for AKI, eGFR <30 or relevant arterial procedures, then reassess after48h. The FDA contrast label is more restrictive.

Start SGLT2i down to eGFR 20, reassure on the 3–5 mL/min dip, counsel on genital mycotic infection/euglycemic DKA/sick-day hold; titrate GLP-1 RA slowly and watch for dehydration-AKI from GI effects

Interpret a low eGFR in an 80-year-old without reflex referral, list who does need nephrology, dose-adjust DOACs/gabapentin/sulfonylureas, and deprescribe NSAIDs and PPIs

Identify a CKM candidate (frail, ≥80, high comorbidity, patient preference), use the surprise question, open a goals-of-care conversation, and name the symptoms to manage without dialysis

Avoid or clear with the center any CYP3A4 drug (azoles, macrolides, diltiazem/verapamil, grapefruit), NSAIDs, allopurinol with azathioprine, and live vaccines; keep up skin and cervical cancer screening; call the transplant center for fever, rising creatinine, reduced urine, diarrhea/vomiting, or any new prescription or admission