When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

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NephrologyChronicCommon

Chronic Kidney Disease (CKD)

Progressive, irreversible loss of nephron function over months to years. Management centers on slowing progression (RAAS blockade + SGLT2i), treating complications (anemia, bone-mineral disease, acidosis), and timely dialysis planning.

🔍 Overview

Definition

CKD is defined as abnormalities of kidney structure or function present for > 3 months with health implications. Requires either GFR < 60 mL/min/1.73m² OR markers of kidney damage (albuminuria, hematuria, structural abnormality, history of transplant) -or both. Classified by GFR stage (G1–G5) and albuminuria category (A1–A3).

GFR Staging (KDIGO)

Stage	GFR (mL/min/1.73m²)	Description	Mortality Risk
G1	≥ 90	Normal or high (with kidney damage markers)	Baseline
G2	60–89	Mildly decreased	Slightly increased
G3a	45–59	Mild-moderately decreased	Moderately increased
G3b	30–44	Moderate-severely decreased	High
G4	15–29	Severely decreased	Very high
G5	< 15	Kidney failure (ESKD)	Highest

Albuminuria Categories

Category	UACR (mg/g)	Description
A1	< 30	Normal to mildly increased
A2	30–300	Moderately increased (microalbuminuria)
A3	> 300	Severely increased (macroalbuminuria) -high ESKD risk

Both GFR and albuminuria independently predict progression and cardiovascular risk. A patient with G2 + A3 is higher risk than G3a + A1. Always classify both.

Etiology (Most Common → Least)

Cause	% of ESKD	Key Features
Diabetes mellitus	~45%	Most common cause worldwide. Nodular glomerulosclerosis (Kimmelstiel-Wilson). Progressive albuminuria → nephrotic range.
Hypertension	~28%	Hypertensive nephrosclerosis. Arteriolar thickening → ischemic nephron loss. Often coexists with DM.
Glomerulonephritis	~8%	IgA nephropathy (most common GN globally), FSGS, membranous, lupus nephritis. Active sediment (RBC casts).
Polycystic kidney disease (ADPKD)	~5%	Autosomal dominant. Bilateral enlarged cystic kidneys on imaging. Family history. Tolvaptan slows progression TEMPO 3:3, 2012.
Other	~14%	Reflux nephropathy, obstructive uropathy, interstitial nephritis, amyloidosis, myeloma kidney, sickle cell.

Pathophysiology

Regardless of cause, CKD follows a common final pathway: initial injury → nephron loss → compensatory hyperfiltration in remaining nephrons → glomerular hypertension → progressive glomerulosclerosis → further nephron loss → cycle continues. RAAS activation drives this cycle -which is why ACEi/ARBs are foundational therapy. SGLT2 inhibitors reduce intraglomerular pressure by restoring tubuloglomerular feedback (constricting the afferent arteriole).

Key concept: After ~50% nephron loss, progression becomes self-sustaining even if the original insult is removed. This is why early intervention (BP control, RAAS blockade, SGLT2i) is critical -you're trying to break the hyperfiltration cycle before it becomes irreversible.

Presentation

Early (G1–G3a): Usually asymptomatic. Detected incidentally on labs (elevated Cr, proteinuria on UA).
Moderate (G3b–G4): Fatigue, nocturia (loss of concentrating ability), mild edema, anemia symptoms, pruritus.
Severe (G5 / ESKD): Uremic symptoms -nausea, anorexia, metallic taste, asterixis, encephalopathy, pericarditis, bleeding diathesis (platelet dysfunction), volume overload, Kussmaul breathing (acidosis).

Uremic emergency: Uremic pericarditis (friction rub), uremic encephalopathy (asterixis, seizures), or refractory volume overload → emergent dialysis indication (AEIOU mnemonic from AKI topic).

🧪 Workup & Diagnosis

Diagnostic Workup

Test	Purpose
BMP (Cr, BUN)	Calculate eGFR (CKD-EPI 2021). Two values ≥ 3 months apart confirm chronicity.
Urinalysis with micro	Proteinuria, hematuria, casts. Active sediment (RBC casts) → GN. Bland sediment → DM/HTN nephrosclerosis.
UACR (spot urine)	Quantify albuminuria. Most important prognostic marker. Repeat × 2 to confirm (transient proteinuria is common).
Renal ultrasound	Kidney size (small bilateral = chronic), echogenicity (increased = fibrosis), cysts (ADPKD), hydronephrosis (obstruction).
CBC	Anemia of CKD (normocytic, normochromic). EPO deficiency begins at G3.
Ca²⁺, PO₄, PTH, Vitamin D (25-OH)	CKD-MBD evaluation. Start monitoring at G3a. Expect: ↓ Ca, ↑ PO₄, ↑ PTH, ↓ Vit D.
Iron studies (ferritin, TSAT)	Iron deficiency is common and must be corrected before EPO agents. Target: ferritin > 100, TSAT > 20%.
Lipid panel	CVD risk assessment. CKD is a coronary risk equivalent.
HbA1c	Glycemic control if diabetic. Note: HbA1c is unreliable in ESKD (shortened RBC lifespan, EPO use).
Hepatitis B/C, HIV	Screen all CKD patients. Hep B vaccination if non-immune (double dose in CKD).

When to Pursue Etiology

Active urine sediment (RBC casts, dysmorphic RBCs) → glomerulonephritis workup: complement levels (C3/C4), ANA, anti-dsDNA, ANCA, anti-GBM, SPEP/UPEP, hepatitis serologies
Nephrotic-range proteinuria (> 3.5 g/day) without DM → consider renal biopsy
Rapidly declining GFR (> 5 mL/min/year) → urgent nephrology referral + biopsy
Family history of kidney disease → ADPKD (US), Alport syndrome (genetic testing)
Young patient with CKD → always pursue cause (GN, reflux, congenital)

Small bilateral kidneys (< 9 cm) on US = chronic, irreversible. Biopsy is usually not helpful at this stage -insufficient tissue. Exceptions: normal-sized kidneys in CKD (think DM nephropathy, amyloid, ADPKD, HIV nephropathy).

🚨 Management

▶ How to Manage CKD Stage by Stage (tap to expand)

Two parallel tracks at every stage: (1) Slow progression with the Big 4 (BP control, ACEi/ARB, SGLT2i, finerenone if diabetic), (2) Manage complications as nephron loss accumulates (anemia, bone-mineral, acidosis, K+, fluid). KDIGO 2024 added finerenone as a 4th pillar in diabetic CKD with albuminuria and pushed the SGLT2i threshold to eGFR 20.

Step 1: Confirm CKD and stage by GFR + albuminuria

Check	What	Why
Confirm chronicity	Two abnormal values (eGFR < 60 or albuminuria) ≥ 3 months apart	A single abnormal BMP could be AKI, dehydration, or contrast. CKD requires chronicity by definition.
Stage by GFR + UACR	Use the "heat map": G1-G5 × A1-A3. A patient with G2A3 is higher risk than G3aA1.	Both axes independently predict ESKD and CV mortality. Staging by GFR alone undercalls risk.
Identify etiology	BMP, UACR, UA with micro, renal US; pursue further if active sediment, nephrotic proteinuria, rapid decline, young patient, or family hx	~45% DM, ~28% HTN, ~8% GN, ~5% ADPKD. Etiology drives some choices (e.g., tolvaptan for rapid ADPKD, immunosuppression for GN).

Step 2: Universal interventions for every CKD patient

Pillar	How	Why
BP control	Target < 130/80 (< 120/80 if proteinuric per KDIGO 2024)	SPRINT and post-hoc CKD subgroup: intensive control reduces mortality without harming kidney function. BP > 130 accelerates progression and CV death.
ACEi or ARB	Maximally titrated to BP target; required if UACR ≥ 30 (A2 or A3) or proteinuric of any cause	Reduces intraglomerular pressure → slows progression and lowers proteinuria 30-50%. RENAAL, IDNT in diabetic CKD; AASK in hypertensive CKD even in Black patients. Expect Cr rise 10-30%, that's hemodynamic, not injury; only stop if > 30% or K+ > 5.5.
SGLT2 inhibitor	Dapagliflozin 10 mg or empagliflozin 10 mg daily; initiate down to eGFR 20, continue until dialysis	DAPA-CKD (2020): 39% reduction in CKD progression. EMPA-KIDNEY (2022): 28% reduction. Benefit independent of diabetes. Expect 3-5 mL/min initial eGFR dip, reverses.
Finerenone (if diabetic + albuminuria)	10 mg daily (20 mg if K+ stable and eGFR ≥ 60); ADD to ACEi/ARB + SGLT2i, don't replace	FIDELIO-DKD (2020): 18% reduction in CKD progression. FIGARO-DKD (2021): 13% reduction in CV death/MACE. Non-steroidal MRA, less gynecomastia and less hyperkalemia than spironolactone. Class I in KDIGO 2024 for diabetic CKD.
Lifestyle	Sodium < 2 g/day, protein 0.6-0.8 g/kg/day (Stage 3+), smoking cessation, weight loss	Each independently slows progression. Don't restrict protein below 0.6 g/kg (sarcopenia risk).
CV risk reduction	Statin for all CKD G3-G5 not on dialysis (SHARP); ASA if established ASCVD; A1c < 7% if young, < 8% if frail/elderly	CKD is a CAD risk equivalent. Most CKD patients die of CV disease, not progress to ESKD.

Step 3: Stage-specific add-ons

Stage	What's New This Stage	Why
G1-G2 (eGFR ≥ 60)	Treat etiology, optimize Big 4, reassess every 6-12 months	Most patients are asymptomatic; the window for slowing progression is widest here. Don't wait for symptoms.
G3a (45-59)	Add CKD-MBD labs (Ca, PO4, PTH, 25-OH Vit D), anemia screening (CBC, iron studies), vaccines (Hep B, pneumococcal, COVID, flu, RSV, Shingrix)	EPO production drops at G3a. PTH starts rising. Hep B vaccination needs the higher CKD dosing (double dose) and works best while eGFR is still high.
G3b (30-44)	Nephrology referral if not already; start discussing future kidney replacement options; avoid nephrotoxins; review medication renal dosing	Two-year median to ESKD if eGFR declines > 3 mL/min/yr at this stage. Referral late is the #1 reason patients arrive at ESKD without a transplant or fistula plan.
G4 (15-29)	Kidney replacement therapy education (HD/PD/transplant). Pre-emptive transplant evaluation if eGFR < 20. Vascular surgery referral for AVF/AVG planning at eGFR ~20.	AVF maturation takes 3-6 months; placing it < 6 months before dialysis means starting with a catheter (higher infection/mortality). Pre-emptive transplant has better outcomes than transplant after dialysis start.
G5 (< 15)	Initiate KRT when uremic (not by GFR alone), or palliative pathway if appropriate; complete transplant workup if not done	IDEAL (2010): early-start dialysis offered no benefit over symptom-driven start. Don't initiate by number alone, watch for AEIOU indications.

Step 4: Manage complications as they appear

Complication	Threshold to Act	How
Anemia of CKD	Hb < 10 g/dL	Iron first (target ferritin > 100, TSAT > 20%). Then ESA (epoetin alfa, darbepoetin) targeting Hb 10-11.5 (NOT > 12, increased CV events in TREAT, CHOIR). Consider HIF-PHI (daprodustat) as oral alternative.
CKD-MBD	PO4 > 4.5, PTH > 2-9× upper limit, low 25-OH D	Dietary phosphate restriction → phosphate binders (sevelamer or lanthanum first; avoid Ca-based if vascular calcification). Vit D analogs (calcitriol or cinacalcet) for secondary hyperparathyroidism.
Metabolic acidosis	HCO3 < 22	Sodium bicarbonate 650 mg PO TID, target HCO3 ≥ 22. Slows progression (UBI, 2014). Veverimer if available.
Hyperkalemia	K+ > 5.5 limiting RAAS	Patiromer or SZC to preserve RAAS rather than discontinue it (DIAMOND, AMBER). Diet education, avoid NSAIDs.
Volume overload	Edema, weight gain, dyspnea	Loop diuretic (furosemide, torsemide); often needs higher doses as eGFR falls. Sodium restriction.
Uremic symptoms	Nausea, pruritus, asterixis, encephalopathy, pericarditis	Indication to initiate dialysis (AEIOU). Pruritus: gabapentin or difelikefalin (kappa-opioid agonist, FDA-approved 2021).

Step 5: KRT preparation in G4-G5

Modality	When to Choose	Why
Pre-emptive kidney transplant	eGFR < 20, no exclusions; refer to transplant center for evaluation	Best long-term outcomes, lowest mortality. Pre-emptive (before dialysis) is better than post-dialysis. Living donor preferred over deceased.
Hemodialysis (HD)	Patient preference, in-center 3×/wk; home HD for some	Highest "rescue" capability for fluid/K+. AVF preferred over AVG over catheter (infection risk catheter >> graft > fistula).
Peritoneal dialysis (PD)	Patient preference, home-based, daily exchanges or cycler at night	Preserves residual kidney function longer, no vascular access needed, more lifestyle flexibility. Not for patients with prior abdominal surgery/adhesions.
Conservative / palliative	Frail elderly, dementia, multiple comorbidities where dialysis won't extend or improve quality of life	In octogenarians with multiple comorbidities, dialysis often doesn't extend life and worsens QoL. Honest conversations early.

Shortcuts that override the ladder

Scenario	Do This	Why
Cr rise > 30% on ACEi/ARB	Hold RAAS; screen for bilateral renal artery stenosis (renal duplex, MRA)	RAS unmasks itself when ACEi/ARB drops perfusion to the post-stenotic kidney. Don't just reflexively stop and move on.
Hyperkalemia on RAAS or finerenone	Try patiromer or SZC first; only stop the renoprotective drug if binders fail	RAAS-blockade and finerenone slow progression. Mortality and ESKD benefit is lost if discontinued. K+ binders preserve the regimen.
ADPKD with rapid progression (eGFR drop > 3 mL/min/yr or significant TKV growth)	Tolvaptan (Jynarque); requires LFT monitoring	TEMPO 3:4 (2012) and REPRISE (2017): tolvaptan slowed eGFR decline and total kidney volume growth. Only disease-modifier in ADPKD.
Diabetic CKD with persistent albuminuria on ACEi+SGLT2i	Add finerenone (titrate based on K+ and eGFR)	FIDELIO-DKD/FIGARO-DKD: additive benefit on top of RAAS+SGLT2i. The 4th pillar for diabetic CKD.
Iodinated contrast in eGFR 30-44	Pre/post hydration (isotonic saline 1-1.5 mL/kg/hr); hold metformin and SGLT2i 48 hr; don't withhold contrast if clinically necessary	Contrast-associated AKI risk in modern era is modest; outdated reflexes to avoid contrast can delay diagnosis. PRESERVE (2018): NAC and bicarb didn't help; isotonic saline is what works.
Pregnancy + CKD	Switch ACEi/ARB to labetalol, nifedipine, or methyldopa; close OB-nephro co-management	ACEi/ARB are teratogenic (renal dysgenesis, oligohydramnios). SGLT2i and finerenone also avoided. Pregnancy itself can accelerate CKD; risk stratify by pre-pregnancy eGFR.
Acute illness / NPO / vomiting / contrast / sepsis	Hold "DRAMA" sick-day meds: Diuretics, RAAS, ARBs/ARNI, Metformin, Anti-inflammatories (NSAIDs); also hold SGLT2i	Volume contraction + these drugs = AKI. Resume once eating/drinking and Cr stable.
AKI on top of CKD	Look for reversible cause (volume, obstruction, nephrotoxin, contrast, infection) before assuming progression	~30% of "CKD progression" is actually superimposed AKI that recovers. Treat the AKI; reassess baseline in 3 months.
Refractory albuminuria despite max ACEi+SGLT2i+finerenone	Confirm adherence; refer for biopsy (GN missed at diagnosis); consider GLP-1 RA (FLOW trial, semaglutide reduced kidney events 24%)	FLOW (2024): semaglutide in diabetic CKD reduced major kidney + CV events 24%. New addition to the toolbox. Biopsy uncovers treatable GN (IgA, FSGS, lupus) in some "diabetic CKD" patients.
"Bad-looking" eGFR in muscular or amputee patient	Use cystatin C-based eGFR (eGFRcr-cys is more accurate)	Creatinine is muscle-mass dependent; low muscle (amputee, elderly, sarcopenia) overestimates eGFR. Cystatin C is muscle-independent. 2021 CKD-EPI race-free equation also recommended.

Cornerstone Therapies -Slow Progression

The "Big 4" that change CKD trajectory: BP control, ACEi/ARB, SGLT2 inhibitor, finerenone (if diabetic CKD). Every CKD patient with albuminuria should be on the first three.

1. BP Control

Target < 120/80 mmHg if proteinuria present SPRINT, 2015. Target < 130/80 for all CKD KDIGO, 2024. First-line: ACEi or ARB (dual RAAS blockade).

2. ACEi / ARB

Foundational therapy if albuminuria (A2 or A3). Reduces intraglomerular pressure, slows progression, reduces proteinuria 30–50%. RENAAL, 2001: losartan reduced ESKD by 28% in diabetic nephropathy. IDNT, 2001: irbesartan similar benefit. Do NOT combine ACEi + ARB ONTARGET, 2008: no additional benefit, increased hyperkalemia + AKI.

Expect Cr to rise 10–30% after initiation -this is acceptable and expected. Only hold if Cr rises > 30% or K⁺ > 5.5.

3. SGLT2 Inhibitor

Add to ACEi/ARB in all CKD with eGFR ≥ 20 and albuminuria. Benefit is independent of diabetes status.
DAPA-CKD, 2020: dapagliflozin reduced CKD progression by 39%. Trial stopped early for efficacy. Benefit in both diabetic and non-diabetic CKD.
EMPA-KIDNEY, 2022: empagliflozin reduced progression by 28%. Benefit down to eGFR 20.
Mechanism: restores tubuloglomerular feedback → constricts afferent arteriole → reduces intraglomerular pressure. Also natriuretic, reduces weight, lowers BP.
Expect initial eGFR dip of 3–5 mL/min (like ACEi) -this is hemodynamic, not injury. Do not stop.

4. Finerenone (Kerendia)

Add in diabetic CKD with persistent albuminuria despite ACEi/ARB + SGLT2i.
FIDELIO-DKD, 2020: 18% reduction in kidney composite endpoint. FIGARO-DKD, 2021: 13% reduction in CV composite.
Non-steroidal MRA -less hyperkalemia than spironolactone. Requires K⁺ < 5.0 and eGFR ≥ 25 to initiate. Monitor K⁺ within 4 weeks.

Lifestyle & Supportive

Dietary sodium restriction -< 2g/day. Enhances efficacy of RAAS blockade and reduces edema/HTN.
Protein intake -0.8 g/kg/day in G3–G5 (not on dialysis). Excessive protein accelerates hyperfiltration.
Glycemic control (DM) -HbA1c < 7% (individualize in elderly/frail). SGLT2i counts toward this.
Smoking cessation -smoking accelerates CKD progression and CV risk.
Statin therapy -CKD is a coronary risk equivalent. Statin for all G3–G5 not on dialysis SHARP, 2011: simvastatin/ezetimibe reduced major atherosclerotic events by 17%.
Avoid nephrotoxins -NSAIDs, aminoglycosides, IV contrast (pre-hydrate if essential), herbal supplements.
Vaccinations -Hepatitis B (double dose: 40 mcg), influenza annually, pneumococcal (PCV20 or PCV15 + PPSV23), COVID-19.

⚠️ Complications

CKD-Mineral Bone Disease (CKD-MBD)

Begins at G3. The kidneys fail to excrete phosphate and activate vitamin D → hyperphosphatemia → hypocalcemia → secondary hyperparathyroidism → renal osteodystrophy → vascular calcification → cardiovascular death.

Parameter	CKD G3–G4	CKD G5 / Dialysis	Treatment
Phosphate	Keep in normal range	Target 3.5–5.5 mg/dL	Dietary restriction → phosphate binders: sevelamer (Renvela), calcium acetate (PhosLo), lanthanum (Fosrenol)
Calcium	Maintain normal	Avoid hypercalcemia	Avoid calcium-based binders if hypercalcemic. Calcitriol (Rocaltrol) or paricalcitol (Zemplar) for active vitamin D.
PTH	Trend -no target	2–9× upper normal	Calcitriol, cinacalcet (Sensipar), or parathyroidectomy if refractory.
Vitamin D (25-OH)	Replete if < 30 ng/mL	Replete	Ergocalciferol or cholecalciferol (inactive form) for deficiency. Active forms for secondary hyperPTH.

Anemia of CKD

EPO production drops as renal mass decreases (begins G3). Results in normocytic, normochromic anemia. Always rule out iron deficiency first.

Step	Action	Target
1. Iron first	IV iron (ferric carboxymaltose or iron sucrose) if ferritin < 100 or TSAT < 20%	Ferritin 200–500, TSAT 20–30%
2. ESA if needed	Epoetin alfa (Epogen/Procrit) or darbepoetin (Aranesp). Start if Hgb < 10 after iron repletion.	Hgb 10–11.5 g/dL. Do NOT target > 13 TREAT, 2009: ↑ stroke risk. CHOIR, 2006: ↑ CV events.
3. HIF-PHI (newer)	Roxadustat (Evrenzo) -oral HIF-prolyl hydroxylase inhibitor. Stimulates endogenous EPO.	Alternative to injectable ESAs. Approved in CKD + dialysis.

Never target Hgb > 13 g/dL with ESAs. TREAT, 2009: doubled stroke risk. CHOIR, 2006: increased CV events. CREATE, 2006: no benefit. Target 10–11.5 only.

Metabolic Acidosis

Impaired ammonium excretion → non-anion-gap metabolic acidosis (early) or anion-gap (late, from retained uremic toxins). Acidosis accelerates CKD progression, worsens bone disease, and promotes muscle wasting.

Target serum bicarb ≥ 22 mEq/L
Sodium bicarbonate tablets 650–1300 mg PO TID (1–3 mEq/kg/day)
Bicarb CKD Progression Trial, 2010: bicarb supplementation slowed CKD progression by 60%

Other Complications

Hyperkalemia -from impaired K⁺ excretion + ACEi/ARB/MRA. Manage with dietary restriction, patiromer (Veltassa), sodium zirconium cyclosilicate (Lokelma). Do NOT stop ACEi/ARB unless K⁺ > 5.5 persistently.
Volume overload / edema -loop diuretics (furosemide). Dose escalation needed as GFR declines. Thiazides lose efficacy below GFR 30 (exception: metolazone for synergy).
Cardiovascular disease -#1 cause of death in CKD. CKD is a coronary risk equivalent. Statin for all SHARP, 2011. Manage HTN aggressively.
Uremic pruritus -gabapentin (renal dose), emollients, UVB phototherapy, difelikefalin (Korsuva) for dialysis patients.
Uremic platelet dysfunction -prolonged bleeding time despite normal PT/INR. Treat with desmopressin (DDAVP) 0.3 mcg/kg IV for acute procedures. Conjugated estrogens for sustained effect.

💊 Medications

CKD-Specific Medications

Drug (Brand)	Class	Dose	Indication	Key Points
Dapagliflozin (Farxiga) 1ST LINE	SGLT2i	10 mg PO daily	CKD with eGFR ≥ 20 + albuminuria	DAPA-CKD, 2020. DM and non-DM. Do not initiate < 20.
Empagliflozin (Jardiance) 1ST LINE	SGLT2i	10 mg PO daily	CKD with eGFR ≥ 20	EMPA-KIDNEY, 2022. Benefits down to eGFR 20.
Finerenone (Kerendia) ADD-ON	Non-steroidal MRA	10–20 mg PO daily	Diabetic CKD with albuminuria despite ACEi/ARB	FIDELIO-DKD, 2020. Requires K⁺ < 5.0 to start. Monitor K⁺ at 4 wks.
Sevelamer (Renvela) PREFERRED	Phosphate binder	800–1600 mg with meals	Hyperphosphatemia (G4–G5)	Non-calcium binder. Preferred over calcium-based binders to avoid vascular calcification.
Calcitriol (Rocaltrol)	Active vitamin D	0.25–0.5 mcg PO daily	Secondary hyperparathyroidism	Monitor Ca²⁺ (risk of hypercalcemia). Alternative: paricalcitol (Zemplar) -less hypercalcemia.
Cinacalcet (Sensipar)	Calcimimetic	30–180 mg PO daily	Secondary hyperPTH on dialysis	Activates CaSR on parathyroid → suppresses PTH. GI side effects common.
Epoetin alfa (Epogen) AFTER IRON	ESA	50–300 units/kg 3×/week IV/SC	Anemia of CKD (Hgb < 10)	Iron-replete first. Target Hgb 10–11.5. Never > 13 TREAT, 2009.
Darbepoetin (Aranesp)	ESA (long-acting)	0.45 mcg/kg q2 weeks or monthly	Anemia of CKD	Less frequent dosing than epoetin. Same Hgb target.
Sodium bicarbonate	Alkali	650–1300 mg PO TID	Metabolic acidosis (bicarb < 22)	Slows CKD progression. Watch for volume overload (Na⁺ content).
Patiromer (Veltassa) ADJUNCT	K⁺ binder	8.4–25.2 g PO daily	Chronic hyperkalemia on RAAS blockade	Allows continuation of ACEi/ARB/MRA. Takes hours to work -not for acute hyperK.

Drug Dosing in Renal Impairment

Renal impairment changes a drug in one of three ways: it becomes unsafe (stop or avoid), it accumulates (reduce the dose or extend the interval), or it needs level-guided dosing. Most drug labels use Cockcroft-Gault creatinine clearance (CrCl calculator), not eGFR, the two diverge at extremes of body size, so dose by CrCl and stage by eGFR. In AKI, kidney function is a moving target, assume the worst, dose conservatively, and recheck daily. Thresholds below are starting points, confirm against the current label for any unfamiliar drug.

1. Stop or avoid (highest-yield list)

Drug	Threshold	Why	Use instead
NSAIDs	Avoid eGFR < 30; avoid prolonged use 30–59	Afferent arteriolar vasoconstriction drops GFR → AKI, hyperkalemia, fluid retention, blunted antihypertensives, faster CKD progression.	Acetaminophen first-line; topical NSAID for localized pain; short low-dose course only if unavoidable.
Metformin	Contraindicated < 30; do not start < 45; if 30–44 cap at 1000 mg/day	Accumulation raises lactic acidosis risk. Also hold around iodinated contrast and acute illness.	SGLT2i or GLP-1 RA (also organ-protective); linagliptin if a gliptin is wanted.
Nitrofurantoin	Avoid CrCl < 30	Low GFR gives inadequate urinary drug levels (treatment failure) plus systemic accumulation and pulmonary/neuro toxicity. Short courses only above 30.	For cystitis: cephalexin or amoxicillin-clavulanate (dose-adjusted); TMP-SMX if CrCl > 30.
Glyburide (sulfonylurea)	Avoid in advanced CKD	Renally cleared active metabolites cause prolonged, dangerous hypoglycemia.	Glipizide (hepatic metabolism) if a sulfonylurea is needed; better, an SGLT2i or DPP-4i.
Spironolactone / eplerenone	Caution eGFR 30–45; avoid < 30	Impaired potassium excretion → hyperkalemia. If used at 30–50, start 25 mg every other day and recheck K⁺.	For diabetic CKD, finerenone (still monitor K⁺); for HTN, a thiazide-like or loop diuretic.
IV bisphosphonates (zoledronate)	Avoid eGFR < 30–35	Dose- and infusion-rate-dependent nephrotoxicity (acute tubular injury).	Denosumab (not renally cleared, no dose adjustment), but watch for hypocalcemia and replete Ca / vitamin D.
Sotalol	Avoid in advanced renal failure	Renally cleared; accumulation prolongs QT → torsades.	Amiodarone (hepatic clearance) for rhythm; metoprolol or diltiazem for rate control.
Gadolinium (group I agents)	Avoid eGFR < 30 and dialysis	Nephrogenic systemic fibrosis.	Newer group II gadolinium agent (NSF risk near zero), lowest dose; or non-contrast MRI.

2. Antibiotics (adjust or monitor)

Drug	What to do	Why	Use instead
Vancomycin	Dose by AUC/levels, extend the interval as CrCl falls	Renally cleared and itself nephrotoxic. Trough/AUC-guided dosing prevents both under-treatment and AKI.	If AKI or level problems: linezolid or daptomycin for MRSA (no renal efficacy penalty; daptomycin interval extended).
Aminoglycosides (gentamicin, tobramycin)	Extend interval, monitor troughs, avoid if an alternative exists	Nephrotoxic (ATN) and ototoxic; toxicity rises with accumulation.	An anti-pseudomonal beta-lactam (cefepime, pip-tazo, meropenem, all dose-adjusted) per susceptibility.
Cefepime	Reduce dose per CrCl	Neurotoxicity (encephalopathy, myoclonus, nonconvulsive status epilepticus); ~85% of cases occur in renal impairment without dose adjustment.	Dose-adjust rather than swap; if neurotoxicity occurs, switch to meropenem or pip-tazo (also adjusted).
Piperacillin-tazobactam	Reduce per CrCl; avoid pairing with vancomycin when possible	The vancomycin + pip-tazo combination is associated with additive AKI.	Swap the pairing to cefepime + vancomycin or meropenem when broad coverage is needed.
Carbapenems (meropenem, imipenem)	Reduce per CrCl	Accumulation lowers the seizure threshold (imipenem most). Also lowers valproate levels.	Meropenem over imipenem (lower seizure risk); dose-adjust rather than swap class if carbapenem is indicated.
Fluoroquinolones	Levofloxacin reduce CrCl < 50; ciprofloxacin < 30	Accumulation → QT prolongation, CNS effects, tendinopathy.	Moxifloxacin (no renal adjustment, hepatic) where the spectrum fits; otherwise a beta-lactam per organism.
TMP-SMX	Reduce dose CrCl < 30	Trimethoprim blocks ENaC (hyperkalemia) and tubular creatinine secretion (a pseudo-rise in Cr, not true AKI). Distinguish before stopping.	Indication-dependent (no universal swap); for UTI use cephalexin, for PJP the dose is reduced rather than substituted.
Acyclovir / valacyclovir	Reduce per CrCl, hydrate, infuse IV slowly	Crystal nephropathy and neurotoxicity (confusion, myoclonus) when not adjusted.	Dose-adjust and hydrate rather than swap; valacyclovir PO over IV acyclovir when oral therapy is appropriate.

3. Anticoagulants

Listed preferred-first. Apixaban is the DOAC of choice in CKD because it is the least renally cleared (~27%); rivaroxaban follows directly to make the contrast obvious (~36% renal, so it is dose-reduced earlier and avoided sooner). Dabigatran is the most kidney-dependent and the first to drop off.

Drug	Threshold / action	Why	Use instead
Apixaban PREFERRED DOAC	Reduce to 2.5 mg BID if 2 of 3: age ≥ 80, weight ≤ 60 kg, Cr ≥ 1.5	Least renally cleared DOAC (~27%), most usable in advanced CKD. Use in dialysis remains debated but it is the DOAC of choice when one is used.	This is the preferred alternative; if a DOAC is unsuitable, warfarin (INR-titrated) remains usable at any GFR.
Rivaroxaban	AFib CrCl 15–50 → 15 mg daily; avoid < 15	More renally cleared than apixaban (~36%), so it accumulates sooner → bleeding. Same Xa-inhibitor class, but apixaban is preferred as function falls.	Apixaban (or warfarin) below CrCl 15.
Dabigatran	75 mg BID if CrCl 15–30; avoid < 30 (contraindicated < 15)	~80% renal clearance, the most kidney-dependent DOAC, so bleeding climbs fastest as function falls.	Apixaban (or warfarin) below CrCl 30.
Edoxaban	Reduce if CrCl 15–50; avoid if CrCl > 95 or < 15	The > 95 paradox: it under-protects against stroke at high clearance, a classic exam point.	Apixaban or rivaroxaban if CrCl > 95; apixaban/warfarin if < 15.
Enoxaparin	Treatment dose 1 mg/kg once daily (not BID) if CrCl < 30; consider anti-Xa monitoring	Renal accumulation → bleeding.	IV unfractionated heparin (titratable, reversible, not renally cleared) in severe renal failure.

4. Diabetes agents

Drug	Threshold / action	Why	Use instead
SGLT2 inhibitors (dapa/empa)	Initiate eGFR ≥ 20 (empagliflozin) or ≥ 25 (dapagliflozin); continue until dialysis	Glucose-lowering fades below ~45, but renal and CV protection persists, so keep them on for the kidney benefit, not the sugar.	Below the initiation threshold, add a GLP-1 RA or linagliptin for glycemic control.
Sulfonylureas	Prefer glipizide; avoid glyburide	Glipizide is hepatically metabolized; glyburide has renally cleared active metabolites causing prolonged hypoglycemia.	Glipizide; or shift to an SGLT2i, GLP-1 RA, or linagliptin.
Insulin	Reduce total daily dose as eGFR falls	The kidney clears insulin; less clearance means longer action and more hypoglycemia.	Same agent, lower dose; favor titratable basal-bolus over fixed mixes for safety.
DPP-4 inhibitors	Reduce sitagliptin/saxagliptin; linagliptin needs no adjustment	Linagliptin is biliary/hepatically cleared, the go-to gliptin in CKD.	Linagliptin (no renal dose adjustment).
GLP-1 agonists	Generally no dose change	Watch for volume depletion from GI losses (nausea, vomiting), which can precipitate prerenal AKI.	No swap needed; hydrate and titrate slowly. A preferred class in CKD.

5. Cardiovascular

Drug	What to do	Why	Use instead
Digoxin	Reduce dose, monitor levels	Narrow therapeutic index and renally cleared; toxicity is worsened by the hypokalemia and hypomagnesemia common in CKD.	For rate control, a beta-blocker or non-DHP calcium channel blocker instead.
Atenolol, nadolol, sotalol	Accumulate as CrCl falls	Renally cleared beta-blockers build up (bradycardia, heart block); the hepatically cleared ones are safer in CKD.	Metoprolol or carvedilol (hepatic clearance, no renal adjustment).
ACEi / ARB	Not dose-reduced, but expect a Cr rise ≤ 30% (acceptable) and watch K⁺; hold during AKI or acute illness (sick-day rule)	Efferent arteriolar dilation drops GFR slightly; only a Cr rise > 30% or hyperkalemia signals true harm. They remain renoprotective long-term.	No swap, they are renoprotective; if intolerant from hyperkalemia, add a K⁺ binder (patiromer) rather than stopping.
Rosuvastatin	Max 10 mg/day if eGFR < 30	Higher systemic exposure in renal impairment raises myopathy/rhabdomyolysis risk.	Atorvastatin (hepatic/biliary clearance, no renal dose cap).

6. Analgesia, neuro, and miscellaneous

Drug	What to do	Why	Use instead
Gabapentin / pregabalin	Reduce ~50% if CrCl < 60; CKD4 (15–29) ~200–700 mg/day; CKD5 or HD 100–300 mg with a dose after dialysis	> 90% renal elimination, accumulation causes sedation, myoclonus, and falls, a very common inpatient error.	Reduce dose rather than swap; for neuropathic pain a tricyclic (nortriptyline) or duloxetine avoids renal accumulation.
Morphine, codeine	Avoid in advanced CKD	The active metabolite morphine-6-glucuronide is renally cleared and accumulates → sedation and respiratory depression.	Hydromorphone or fentanyl (fentanyl is the safest opioid in renal failure).
Tramadol	Reduce dose	Metabolite accumulation plus a lowered seizure threshold.	Fentanyl or low-dose hydromorphone for opioid-requiring pain.
Allopurinol	Start low (50–100 mg), titrate to the urate target with monitoring	The active metabolite oxypurinol accumulates and can trigger allopurinol hypersensitivity syndrome (DRESS, SJS/TEN). Slow titration, not a fixed low cap, is current practice.	Febuxostat (hepatic metabolism, no renal dose adjustment); note the CARES CV-mortality signal, weigh in cardiac patients.
Colchicine	Reduce or avoid; never combine with a strong CYP3A4/P-gp inhibitor in renal failure	Accumulation → myoneuropathy and marrow suppression.	For acute gout, corticosteroids (oral or intra-articular); IL-1 inhibitor if refractory.
Lithium	Monitor levels closely, avoid volume depletion	Narrow index, renally cleared, and itself nephrotoxic (nephrogenic DI, chronic interstitial nephritis).	If nephrotoxicity develops, an alternative mood stabilizer (e.g., valproate, lamotrigine) in conjunction with psychiatry.
Iodinated contrast	Hydrate, minimize volume, hold metformin around the study	Contrast-associated AKI risk rises with lower baseline GFR.	Non-contrast CT/ultrasound, or MRI with a group II gadolinium agent, when feasible.

🏥 Dialysis & Transplant

When to Start Dialysis

Mnemonic: AEIOU -Same as AKI. Initiate when medical management fails, not based on a GFR number alone.

Indication	Details
A -Acidosis	Refractory metabolic acidosis despite oral bicarb
E -Electrolytes	Refractory hyperkalemia despite binders + dietary restriction
I -Intoxication	Uremic encephalopathy, uremic pericarditis (absolute indication)
O -Overload	Refractory volume overload despite max diuretics
U -Uremia	Symptomatic uremia (nausea, anorexia, asterixis, neuropathy) -typically GFR 5–10

Do NOT start dialysis based on GFR alone. IDEAL, 2010: early dialysis initiation (GFR 10–14) vs late (GFR 5–7) showed no survival benefit. Start for symptoms or complications, not a number.

Dialysis Modalities

Modality	Access	Schedule	Best For	Disadvantages
Hemodialysis (HD)	AV fistula (best) > AV graft > tunneled catheter (worst)	3×/week, 3–4 hrs/session	Most ESKD patients. Rapid solute/fluid removal.	Hemodynamic instability, vascular access complications, in-center schedule burden.
Peritoneal dialysis (PD)	Tenckhoff catheter (peritoneal)	Daily exchanges (CAPD) or nightly cycler (APD)	Patient autonomy, home-based, preserves residual renal function longer, better for hemodynamically fragile patients.	Peritonitis risk, protein loss, not ideal if prior abdominal surgery/hernias.
CRRT	Temporary dialysis catheter	Continuous (ICU only)	Hemodynamically unstable ICU patients (septic shock). Gentler fluid/solute removal.	ICU-only, resource intensive, requires anticoagulation of circuit.

Access Planning

AV fistula referral at eGFR ~20 (G4) -needs 2–3 months to mature before use. "Fistula first" approach.
Protect the non-dominant arm -no blood draws, no IVs, no BP cuffs on the future fistula arm from G4 onwards.
Avoid subclavian lines -causes subclavian stenosis, makes future fistula/graft on that side impossible. Use IJ if central access needed.
Transplant evaluation -refer when GFR < 20. Pre-emptive transplant (before dialysis) has best outcomes. Living donor preferred.

BP target in ESRD: SBP, not MAP

For chronic dialysis BP management, follow SBP, not MAP. Vascular calcification widens pulse pressure in dialysis patients, so a "normal" MAP can hide a damaging SBP. Example: BP 180/60 gives MAP 100 (looks fine) but that 180 SBP is hammering the brain and heart every beat. KDOQI and KDIGO target SBP. Caveat: in acute settings (intra-dialytic crash, sepsis, peri-op), MAP still rules for organ perfusion.

📋 On Rounds

Pimp Questions

Why should you never combine ACEi + ARB in CKD?

ONTARGET, 2008: dual RAAS blockade (ramipril + telmisartan) vs either alone -no additional renal benefit, but significantly more hyperkalemia, hypotension, and acute kidney injury. Also: VA NEPHRON-D, 2013 stopped early for safety (losartan + lisinopril in diabetic nephropathy). Bottom line: one RAAS blocker is enough. If more antiproteinuric effect needed, add SGLT2i or finerenone.

Why does eGFR dip when you start an SGLT2 inhibitor?

SGLT2 inhibitors restore tubuloglomerular feedback -they increase sodium delivery to the macula densa, which signals afferent arteriolar constriction, reducing intraglomerular pressure. This is the therapeutic mechanism (same concept as ACEi reducing efferent tone). The initial eGFR dip of 3–5 mL/min reflects reduced hyperfiltration, not kidney injury. It stabilizes within weeks and long-term GFR slope is markedly better.

Why is HbA1c unreliable in ESKD?

Two reasons: (1) EPO/ESA therapy → increased reticulocyte production → younger RBCs → shorter glycation time → falsely LOW HbA1c. (2) Uremia → carbamylated hemoglobin → can interfere with some assays → falsely HIGH. Also, shortened RBC lifespan in ESKD (90 vs 120 days) → less glycation time. Alternative: use glycated albumin or fructosamine for glycemic monitoring in ESKD.

When should you refer for AV fistula creation?

At eGFR ~20 (CKD G4), or ~12 months before anticipated dialysis start. AV fistulas need 2–3 months to mature (some need 6 months). "Fistula first" -AVF has lowest infection rate, best long-term patency, and lowest mortality compared to grafts or catheters. Protect the non-dominant arm from G4 onwards (no IVs, no blood draws, no BP cuffs). Avoid subclavian central lines -causes stenosis that ruins ipsilateral fistula options.

Should you start dialysis early based on GFR alone?

No. IDEAL, 2010: randomized early start (eGFR 10–14) vs late start (eGFR 5–7) in 828 patients -no difference in mortality, CV events, infections, or quality of life. Early start just means more time on dialysis with no survival benefit. Start dialysis for symptoms (uremia, refractory volume overload, refractory hyperK, pericarditis) -not a number.

Clinical Examples

Case 1: CKD Stage 3b with Albuminuria

Presentation: 62M with T2DM and HTN. eGFR 38, UACR 450 mg/g, BP 134/82. Currently on Lisinopril (Prinivil) 40 mg daily.

Key Decisions:

Add Dapagliflozin (Farxiga) 10 mg daily, DAPA-CKD, 2020 showed 39% reduction in CKD progression regardless of diabetes status
Add Finerenone (Kerendia) 10–20 mg daily, FIDELIO-DKD, 2020 reduced CKD progression and CV events in diabetic kidney disease
Expect initial eGFR dip of 3–5 mL/min after starting SGLT2i, this is the therapeutic mechanism (tubuloglomerular feedback), not injury. Continue if dip < 30% and stable.
Monitor potassium at 2–4 weeks after starting finerenone (hold if K⁺ > 5.5 at initiation)
Nephrology referral now, eGFR < 30 threshold approaching; early referral allows time for fistula planning if trajectory continues

Teaching point: SGLT2i + finerenone + ACEi/ARB triple combination is now guideline-supported for CKD with albuminuria and DM. Do NOT add ARB on top of ACEi (ONTARGET).

Case 2: CKD Stage 4, Pre-Dialysis Planning

Presentation: 75F with CKD G4. eGFR 18. Labs: bicarb 18, K⁺ 5.6, Hgb 9.2, PTH 310, PO₄ 5.4.

Active Problem List and Plan:

Metabolic acidosis (bicarb 18): Start Sodium Bicarbonate 650 mg TID, target bicarb ≥ 22 (slows CKD progression per de Brito-Ashurst, 2009)
Anemia (Hgb 9.2): Check iron studies first, replete iron (IV iron preferred if TSAT < 20%). If iron-replete, start Epoetin Alfa (Epogen) or Darbepoetin (Aranesp); target Hgb 10–11
Hyperkalemia (K⁺ 5.6): Dietary potassium restriction + consider Patiromer (Veltassa) to allow continuation of RAAS blockade
Secondary hyperPTH (PTH 310, PO₄ 5.4): Start phosphorus binder (e.g., Sevelamer (Renvela) 800 mg TID with meals)
AV fistula referral, eGFR 18 means dialysis likely within 1–2 years; fistula needs 3–6 months to mature
Modality discussion: Address HD vs PD vs transplant. Transplant eval at eGFR ~20. PD preferred if preserved residual function and self-care capable.

Teaching point: CKD G4 is a system, address all complications simultaneously. Do not defer anemia, acidosis, or MBD management while waiting for dialysis.

Case 3: Acute-on-Chronic Kidney Injury

Presentation: 55M with baseline CKD G3 (Cr 1.8). Admitted with Cr 4.2 after 5 days of ibuprofen for back pain + nausea/vomiting with poor PO intake.

Immediate Management:

Hold nephrotoxins immediately: Stop all NSAIDs, hold ACEi/ARB, hold metformin (if applicable)
IV fluids cautiously: NS or LR at 100–150 mL/hr to restore euvolemia, reassess frequently; avoid volume overload in underlying CKD
Monitor closely: Daily BMP (K⁺, bicarb, Cr), urine output. Watch for hyperkalemia and need for emergent dialysis (AEIOU criteria)
Trend creatinine: If Cr begins to fall within 48–72 hrs → AKI superimposed on CKD. If plateau or worsening → consider intrinsic AKI (NSAID-induced AIN) vs true CKD progression
Renal recovery window: Do NOT restart ACEi/ARB until Cr returns to within 25% of baseline and patient euvolemic
Distinguish AKI from CKD progression: True CKD progression requires eGFR decline > 5 mL/min/yr over ≥ 3 months, a single elevated Cr in an ill patient is not CKD progression

Teaching point: NSAIDs reduce prostaglandin-mediated afferent arteriolar dilation, in CKD, this causes acute hemodynamic AKI. This is the #1 avoidable AKI cause in CKD patients. Counsel all CKD patients to avoid NSAIDs absolutely.

Sample Presentation

📋 CKD -Outpatient Nephrology

"Mr. Patel is a 58-year-old man with Type 2 DM, HTN, and CKD Stage G3b-A3 (eGFR 38, UACR 820 mg/g). He is on lisinopril 40 mg daily, dapagliflozin 10 mg daily, and was recently started on finerenone 10 mg daily -K⁺ was 4.6 at 4-week check. His BP today is 128/76. Labs show Hgb 10.8, bicarb 21, Ca 8.9, PO₄ 4.8, PTH 128, 25-OH Vitamin D 18. Plan: start sodium bicarb 650 mg TID for acidosis, replete Vitamin D with ergocalciferol 50,000 units weekly × 8 weeks, recheck PTH/Ca/PO₄ in 3 months. AV fistula referral placed. Transplant evaluation in progress."

Monitoring Parameters -Chronic Kidney Disease

Parameter	Frequency	Target / Action
eGFR and UACR	q3–6 months	Track progression rate. eGFR decline > 5 mL/min/year = rapid progression → reassess treatment, nephrology referral. UACR reduction with ACEi/ARB/SGLT2i = treatment working.
BMP (K+, bicarb, Ca, PO4)	q3–6 months (more often in G4–G5)	K+ < 5.5 (on RAAS blockade). Bicarb ≥ 22 (supplement if low). Ca/PO4 for CKD-MBD monitoring.
PTH	Annually (G3–G4), q3–6mo (G5/dialysis)	Rising PTH = secondary hyperparathyroidism → add phosphate binders, calcitriol, cinacalcet. Target 2–9x ULN on dialysis.
CBC (anemia)	q3–6 months	Hgb trending -anemia of CKD begins at G3. If Hgb < 10 → check iron studies → replete iron → then ESA if needed.
Iron studies (ferritin, TSAT)	q3–6 months	Ferritin > 100 (or > 200 on dialysis), TSAT > 20%. Iron-replete before starting ESA.
HbA1c (if diabetic)	q3 months	Target < 7% (individualize). Note: HbA1c unreliable in ESKD (shortened RBC lifespan, EPO use) -use fructosamine or CGM.
BP	Every visit + home monitoring	Target < 130/80 (KDIGO 2024). < 120/80 if tolerated with proteinuria SPRINT, 2015.
Lipids	Annually	CKD is a coronary risk equivalent. Statin for all G3–G5 not on dialysis.
Urinalysis	Annually	Monitor for active sediment (new hematuria, worsening proteinuria).
Hepatitis B/C screening	At diagnosis, then periodically	All CKD patients. Hep B vaccination if non-immune (double dose: 40 mcg).
Bone density (DEXA)	Consider in G3–G5 with fracture risk	CKD-MBD causes renal osteodystrophy. DEXA interpretation is complex in CKD -discuss with nephrology.

CKD monitoring is a system. Every visit: BP, eGFR trend, UACR, K+, bicarb. Every 3–6 months: CBC, iron, Ca/PO4/PTH. Annually: lipids, HbA1c, UA, Hep B/C. Adjust medications based on trends, not single values.