CNN-NP cheat sheet

CKD is defined as abnormalities of kidney structure or function present for >3 months with health implications; staging uses GFR category G1-G5 combined with albuminuria category A1-A3 (KDIGO heat map).

CKD-EPI 2021 creatinine equation is race-free and recommended over the 2009 equation; eGFR <60 mL/min/1.73 m2 for >3 months defines CKD G3a or worse, and eGFR <15 defines G5.

Albuminuria staging: A1 <30 mg/g, A2 30-300 mg/g, A3 >300 mg/g on spot urine albumin-to-creatinine ratio; confirm with a second specimen over 3-6 months because transient elevation is common.

AKI (KDIGO): creatinine rise >=0.3 mg/dL within 48 h, or >=1.5x baseline within 7 days, or urine output <0.5 mL/kg/h for 6 h; stage 3 includes creatinine >=3.0x baseline, >=4.0 mg/dL, or initiation of RRT.

Hyperkalemia ECG progression: peaked T waves -> PR prolongation -> loss of P waves -> QRS widening -> sine wave; treat with IV calcium first if ECG changes are present, then insulin/glucose or beta-agonist to shift, then removal.

Metabolic acidosis in CKD is typically normal-anion-gap; oral sodium bicarbonate is considered when serum HCO3 is <18-22 mEq/L, with monitoring for sodium load, volume overload, and hypokalemia.

Anemia of CKD: normocytic normochromic; check iron studies before ESA; TSAT <=30% and ferritin <=500 ng/mL (non-dialysis) suggest iron deficiency; ESA is generally not initiated when Hb >=10 g/dL.

CKD-MBD monitoring: serum calcium, phosphate, PTH, and 25-hydroxyvitamin D; trends and PTH targets are interpreted by CKD stage (higher PTH targets in G5 dialysis than in G3-G4).

Peritoneal dialysis prescription terms: fill volume, dwell time, number of exchanges, and solution dextrose concentration (1.5%, 2.5%, 4.25%); higher dextrose increases ultrafiltration and glucose absorption.

Peritonitis in PD is suspected with cloudy effluent, abdominal pain, or fever; diagnosis requires effluent cell count >100 WBC/mm3 with >50% neutrophils plus Gram stain and culture; empiric intraperitoneal antibiotics cover gram-positive and gram-negative organisms.

Hemodialysis adequacy uses Kt/V; a common target is single-pool Kt/V >=1.2 per session for thrice-weekly HD, and urea reduction ratio (URR) >=65%.

AV fistula maturation typically requires 6-8 weeks before first cannulation; the rule of 6s: flow >600 mL/min, diameter >0.6 cm, depth <0.6 cm.

Hemodialysis access infection: arteriovenous graft or fistula with overlying cellulitis or drainage warrants blood cultures and empiric antibiotics; a tunneled catheter with unexplained bacteremia should raise suspicion for catheter-related bloodstream infection.

Dialysis disequilibrium syndrome presents with headache, nausea, confusion, seizures, or coma during or after dialysis; prevention uses slower blood flow, shorter initial sessions, and higher sodium dialysate in high-risk patients.

Intradialytic hypotension: define by a fall in systolic BP >=20 mmHg or MAP >=10 mmHg with symptoms; assess dry weight, ultrafiltration rate, and cardiac function before adjusting antihypertensives.

Hyperphosphatemia management in dialysis: dietary phosphate restriction plus phosphate binders taken with meals; calcium-based binders are limited when hypercalcemia is present.

Nephrotic syndrome: proteinuria >3.5 g/day, hypoalbuminemia, edema, and hyperlipidemia; complications include thrombosis (especially membranous nephropathy), infection, and vitamin D deficiency.

Nephritic syndrome: hematuria with dysmorphic RBCs and RBC casts, hypertension, oliguria, and variable proteinuria; post-streptococcal GN follows pharyngitis by 1-3 weeks or impetigo by 3-6 weeks with low C3.

IgA nephropathy is the most common primary glomerulonephritis worldwide; it presents with episodic gross hematuria after upper respiratory infection, and serum complement is typically normal.

Minimal change disease is the most common nephrotic syndrome in children; it responds to corticosteroids, and biopsy shows normal light microscopy with podocyte foot process effacement on electron microscopy.

Membranous nephropathy in adults is often associated with anti-PLA2R antibodies; it is the most common cause of nephrotic syndrome in older adults and carries a high thrombotic risk.

Rapidly progressive glomerulonephritis presents with declining GFR over days to weeks and crescents on biopsy; anti-GBM disease and ANCA-associated vasculitis are key causes requiring urgent nephrology involvement.

Lupus nephritis is classified by ISN/RPS class I-VI; class III and IV are proliferative and require immunosuppression, and proteinuria plus active urine sediment warrant biopsy.

Alport syndrome: X-linked in most cases (COL4A5), presenting with hematuria, progressive kidney failure, sensorineural hearing loss, and anterior lenticonus.

Hyperkalemia treatment sequence: IV calcium gluconate for membrane stabilization, insulin with glucose and/or albuterol to shift potassium intracellularly, then removal via diuretics, binders, or dialysis.

Hyponatremia correction limits: no more than 8-10 mEq/L in 24 h and 18 mEq/L in 48 h to reduce osmotic demyelination risk; use 3% saline with frequent sodium checks in symptomatic cases.

Hypernatremia correction should not exceed 10-12 mEq/L per 24 h to avoid cerebral edema; free water deficit = total body water x (Na/140 - 1), with TBW about 0.6 x weight in men and 0.5 in women.

Hypokalemia ECG changes: flattened T waves, ST depression, prominent U waves; severe hypokalemia can cause rhabdomyolysis, ileus, and arrhythmias.

Tumor lysis syndrome: hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia; prevention uses hydration and allopurinol or rasburicase for high risk.

Rhabdomyolysis: CK elevation with myoglobinuria, dark urine, and AKI; treat with aggressive IV fluids and monitor for hyperkalemia and hypocalcemia.

Contrast-associated AKI: risk factors include CKD, diabetes, dehydration, and high contrast volume; use lowest effective volume and hold nephrotoxins when feasible.

Diuretic resistance in heart failure or nephrotic syndrome: consider sequential nephron blockade, higher loop doses, or adding a thiazide-like diuretic with close monitoring of electrolytes and renal function.

Kidney transplant immunosuppression typically includes an induction agent (basiliximab or antithymocyte globulin), a calcineurin inhibitor (tacrolimus or cyclosporine), an antimetabolite (mycophenolate), and corticosteroids.

Tacrolimus requires therapeutic drug monitoring; trough goals vary by time post-transplant and rejection risk, and nephrotoxicity plus tremor are common adverse effects.

Acute rejection presents with rising creatinine, decreased urine output, fever, or graft tenderness; biopsy with Banff classification is required to distinguish cellular from antibody-mediated rejection.

BK polyomavirus nephropathy: monitor plasma BK viral load at intervals after transplant; sustained high viral load warrants reducing immunosuppression, and biopsy is used to confirm.

Cytomegalovirus in transplant recipients: prophylaxis with valganciclovir for high-risk serostatus (D+/R-); active disease presents with fever, leukopenia, and organ involvement.

Post-transplant hypertension and diabetes are common; calcineurin inhibitors, corticosteroids, and sirolimus contribute to hyperglycemia and dyslipidemia.

Recurrent disease after transplant: IgA nephropathy, focal segmental glomerulosclerosis, and membranous nephropathy can recur and cause graft dysfunction.

Live kidney donor evaluation includes GFR, albuminuria, blood pressure, glucose tolerance, and infectious disease screening; donors need long-term monitoring of kidney function and blood pressure.

Urinalysis interpretation: RBC casts indicate glomerular bleeding; WBC casts suggest pyelonephritis or interstitial nephritis; muddy brown casts suggest acute tubular necrosis; fatty casts suggest nephrotic syndrome.

Fractional excretion of sodium (FENa) = (urine Na x serum creatinine) / (serum Na x urine creatinine) x 100; FENa <1% suggests prerenal state, but diuretics can raise it.

Urine osmolality >500 mOsm/kg and urine Na <20 mEq/L favor prerenal azotemia; urine osmolality <350 mOsm/kg and urine Na >40 mEq/L favor intrinsic renal injury.

BUN-to-creatinine ratio >20:1 suggests prerenal azotemia or upper GI bleeding; a ratio of 10:1 to 20:1 is typical of normal kidney function.

Serum cystatin C can estimate GFR when creatinine is confounded by muscle mass; the CKD-EPI 2021 creatinine-cystatin C equation is used when confirmation is needed.

24-hour urine protein is the reference for quantifying proteinuria; spot protein-to-creatinine ratio or albumin-to-creatinine ratio is used for screening and monitoring.

Serum complement: low C3 with low C4 suggests lupus nephritis or cryoglobulinemia; low C3 with normal C4 suggests post-streptococcal GN, membranoproliferative GN, or C3 glomerulopathy.

Kidney biopsy complications: bleeding, hematoma, and arteriovenous fistula; hold antiplatelets and anticoagulants per protocol and monitor hemoglobin and vital signs after the procedure.

ACE inhibitors and ARBs reduce proteinuria and slow CKD progression in patients with albuminuria; monitor creatinine and potassium within 1-2 weeks of initiation or dose change.

SGLT2 inhibitors (dapagliflozin, empagliflozin) reduce CKD progression and heart failure hospitalization in CKD with or without diabetes; eGFR decline of up to 30% after initiation is acceptable.

Finerenone, a nonsteroidal mineralocorticoid receptor antagonist, reduces CKD progression and cardiovascular events in type 2 diabetes with albuminuria; monitor potassium.

GLP-1 receptor agonists reduce albuminuria and cardiovascular events in type 2 diabetes; they are an option when metformin and SGLT2 inhibitors are insufficient.

Loop diuretics are preferred over thiazides when eGFR is <30 mL/min/1.73 m2; thiazide-like diuretics remain effective in combination for diuretic resistance.

NSAIDs should be avoided in CKD, especially with ACE inhibitors or ARBs and diuretics (the triple whammy); they cause afferent arteriolar vasoconstriction and AKI.

Metformin is generally continued in CKD G3 but dose-adjusted; it is contraindicated when eGFR <30 mL/min/1.73 m2 because of lactic acidosis risk.

Vaccination and preventive care in CKD: hepatitis B, influenza, pneumococcal, and COVID-19 vaccines; adjust dosing of renally cleared medications and avoid nephrotoxins.

Patient education for CKD includes blood pressure control, sodium and protein moderation, avoidance of NSAIDs and herbal supplements, and recognition of volume overload.

Dialysis access care: check thrill and bruit daily, avoid BP measurement and venipuncture in the access arm, and report redness, swelling, or absent thrill immediately.

Peritoneal dialysis training includes sterile technique, exchange steps, exit-site care, and recognition of peritonitis (cloudy effluent, abdominal pain, fever).

Advance care planning in kidney failure: discuss goals of care, dialysis versus conservative kidney management, and advance directives before crisis.

Medication reconciliation in nephrology: review all prescriptions, over-the-counter drugs, and supplements for nephrotoxicity and dosing by eGFR.

Fluid and sodium education in heart failure with CKD: daily weights, fluid restriction when indicated, and reporting weight gain >2-3 lb/day or 5 lb/week.

Transplant patient education: adherence to immunosuppressants, sun protection, infection precautions, and reporting fever, decreased urine output, or graft tenderness.

Health literacy and teach-back: confirm understanding of medication schedules and dialysis plans, and use interpreters when needed to reduce errors.