ABP Pediatric Nephrology cheat sheet

Nephrotic syndrome: edema, urine protein-to-creatinine ratio >2 mg/mg, albumin <2.5 g/dL, hyperlipidemia; minimal change disease accounts for 80-90% of cases in children aged 1-10 years.

First-line therapy for steroid-sensitive nephrotic syndrome: prednisone 60 mg/m²/day (max 60 mg/day) for 4-6 weeks, then 40 mg/m² on alternate days for 4-6 weeks.

Renal biopsy is indicated for nephrotic syndrome with age <1 or >12 years, hypertension, hematuria, low C3, elevated creatinine, or steroid resistance.

Post-streptococcal GN shows low C3 with normal C4, hematuria, hypertension, and edema 1-3 weeks after pharyngitis; C3 normalizes within 6-8 weeks.

IgA nephropathy causes synpharyngitic gross hematuria with normal complement; it is the most common primary glomerulonephritis worldwide.

Hemolytic uremic syndrome: Shiga toxin-producing E. coli O157:H7, triad of microangiopathic hemolytic anemia, thrombocytopenia, and AKI; supportive care with dialysis when needed; avoid antibiotics and antimotility agents.

Alport syndrome: X-linked COL4A5 mutation, hematuria, progressive CKD, sensorineural hearing loss, anterior lenticonus; ACE inhibitors slow progression.

Hyponatremia correction limit: 8-10 mEq/L per 24 hours to avoid osmotic demyelination; 3% saline is reserved for seizures or severe symptoms.

Anion gap = Na − (Cl + HCO3), normal 8-12 mEq/L; corrected AG = AG + 2.5 × (4.0 − albumin in g/dL).

Type 1 (distal) RTA: urine pH >5.5, hypokalemia, nephrocalcinosis; type 2 (proximal) RTA: bicarbonaturia with urine pH <5.5 once bicarbonate is depleted; type 4 RTA: hyperkalemia with hypoaldosteronism.

Hyperkalemia with ECG changes: give IV calcium gluconate first; then insulin plus glucose, albuterol, and sodium bicarbonate shift K+ intracellularly; remove K+ with binders or dialysis.

A 1 mEq/L fall in serum potassium reflects a total-body deficit of roughly 200-400 mEq.

Normal saline (0.9% NaCl) produces hyperchloremic non-anion-gap metabolic acidosis by diluting bicarbonate and raising chloride.

Bartter syndrome: hypokalemic metabolic alkalosis, hypercalciuria, polyuria, normal blood pressure; Gitelman syndrome: hypocalciuria and hypomagnesemia.

SIADH: euvolemic hypo-osmolar hyponatremia with urine osmolality >100 mOsm/kg and urine Na >40 mEq/L; treat with fluid restriction.

Pediatric hypertension: ≥95th percentile for age, sex, and height on three occasions; stage 1 = 95th to <99th percentile +5 mmHg; stage 2 = ≥99th percentile +5 mmHg.

Renal parenchymal disease is the most common cause of secondary hypertension in children; renovascular disease is the most common cause of severe refractory hypertension in young children.

Coarctation of the aorta: upper-extremity hypertension, lower-extremity hypotension, diminished femoral pulses, and associated bicuspid aortic valve.

Renovascular lesions occur with fibromuscular dysplasia, neurofibromatosis type 1, and Williams syndrome; screen with MRA or CTA.

ACE inhibitors and ARBs are contraindicated in bilateral renal artery stenosis or in a solitary kidney with renal artery stenosis.

Hypertensive emergency: reduce blood pressure by no more than 25% in the first 8 hours; use IV labetalol, nicardipine, or esmolol infusions.

Ambulatory blood pressure monitoring distinguishes white coat hypertension from true hypertension and detects nocturnal non-dipping.

KDIGO AKI: creatinine rise ≥0.3 mg/dL within 48 hours, ≥1.5× baseline within 7 days, or urine output <0.5 mL/kg/h for 6 hours.

FENa = (urine Na × plasma Cr)/(plasma Na × urine Cr) × 100; <1% suggests prerenal AKI, >2% suggests intrinsic renal injury; unreliable after diuretics.

Emergent dialysis indications: refractory hyperkalemia, pulmonary edema, severe metabolic acidosis, uremic encephalopathy or pericarditis, and removable toxins.

Tumor lysis syndrome: hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia; treat with aggressive hydration and rasburicase for hyperuricemia.

Rhabdomyolysis: CK >5 times normal, myoglobinuria, and AKI from pigment nephropathy; treat with isotonic fluid resuscitation and monitor electrolytes.

Contrast-associated AKI prevention: use the lowest volume of low-osmolar contrast plus isotonic saline; bicarbonate and N-acetylcysteine have no proven benefit.

CRRT is preferred over intermittent hemodialysis in hemodynamically unstable children with AKI or severe fluid overload.

KDIGO CKD stages by GFR: G1 ≥90, G2 60-89, G3a 45-59, G3b 30-44, G4 15-29, G5 <15 mL/min/1.73 m².

CKD-mineral bone disease: phosphate retention and low calcitriol cause hypocalcemia and secondary hyperparathyroidism; treat with dietary phosphate restriction, phosphate binders, and active vitamin D.

Anemia of CKD: normocytic normochromic with low erythropoietin; correct iron stores before starting an ESA; target hemoglobin 11-12 g/dL.

Metabolic acidosis in CKD: give oral sodium bicarbonate to maintain serum bicarbonate ≥22 mEq/L, which slows progression and improves growth.

Growth failure in CKD: optimize nutrition and energy intake first; use recombinant growth hormone at 0.05 mg/kg/day subcutaneously if height velocity remains low.

Energy and protein needs on dialysis: energy at 100% of estimated requirement; protein at 100-140% of RDA to offset dialytic losses.

Hyperkalemia in CKD: dietary potassium restriction, potassium binders, and correction of metabolic acidosis.

Peritoneal dialysis fill volume: 30-40 mL/kg body weight, with dwell times adjusted by peritoneal equilibration testing.

PD peritonitis: cloudy effluent, abdominal pain, effluent WBC >100/mm³ with >50% neutrophils; treat with intraperitoneal vancomycin plus a third-generation cephalosporin.

Hemodialysis clearance target: Kt/V ≥1.2 per session, monitored monthly.

Arteriovenous fistula is the preferred hemodialysis access in children weighing >20 kg and requires 6-8 weeks to mature.

Dialysis disequilibrium syndrome: cerebral edema from rapid urea clearance during early sessions; prevent with shorter, slower first sessions and mannitol.

CRRT modalities: CVVH (convection), CVVHD (diffusion), CVVHDF (both); continuous therapy provides gentler fluid and solute removal.

Peritoneal dialysis is preferred in infants and small children because it avoids vascular access and provides better hemodynamic stability.

Most common pediatric kidney transplant is from a living related donor; preemptive transplantation before dialysis yields the best outcomes.

Induction therapy: basiliximab (IL-2 receptor antagonist) for low-risk patients or antithymocyte globulin for high immunologic risk.

Maintenance immunosuppression: tacrolimus, mycophenolate mofetil, and corticosteroids; tacrolimus trough target is roughly 8-12 ng/mL in the first months.

Acute cellular rejection: rising creatinine, fever, graft tenderness; biopsy shows interstitial inflammation and tubulitis; treat with pulse methylprednisolone.

Calcineurin inhibitor toxicity: nephrotoxicity, hypertension, hyperkalemia, hypomagnesemia, and tremor; differentiate from rejection by biopsy.

BK virus nephropathy: screen with urine decoy cells and plasma PCR; reduction of immunosuppression is the primary treatment.

CMV prophylaxis with valganciclovir for 3-6 months in seronegative recipients of seropositive grafts (D+/R−).

Ureteropelvic junction obstruction is the most common cause of antenatal hydronephrosis; MAG3 diuretic renography assesses drainage.

Vesicoureteral reflux is graded I-V by VCUG; grade I involves the ureter only and grade V shows gross dilation and tortuosity; management ranges from observation to prophylaxis and surgery.

Posterior urethral valves: the most common cause of lower urinary tract obstruction in boys; bilateral hydronephrosis, thick-walled bladder, and keyhole urethra; treat with catheter drainage and valve ablation.

Multicystic dysplastic kidney: nonfunctioning kidney replaced by cysts; follow with ultrasound and blood pressure checks; contralateral UPJ obstruction may coexist.

Autosomal recessive polycystic kidney disease: PKHD1 mutation, enlarged echogenic kidneys, congenital hepatic fibrosis, and Potter sequence in severe cases.

Autosomal dominant polycystic kidney disease: PKD1 or PKD2 mutations; hypertension, hematuria, and cysts in adulthood.

Horseshoe kidney: fusion of the lower poles; increased risk of UPJ obstruction, stones, and Wilms tumor.

Nephrogenic diabetes insipidus: AVPR2 or aquaporin-2 mutation; polyuria, dilute urine, hypernatremia; treat with low-solute diet, thiazide diuretics, and amiloride.