ABP Pediatric Nephrology key terms

A clinical tetrad of heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia caused by increased glomerular permeability. Most children have minimal change disease and respond to corticosteroids.

Glomeruli appear normal by light microscopy, with foot-process effacement on electron microscopy. It causes most childhood steroid-sensitive nephrotic syndrome and usually relapses.

Sclerosis of some glomeruli, involving only part of each tuft. It may be primary, genetic, or secondary, and is a common cause of steroid-resistant nephrotic syndrome in children.

Mesangial deposition of IgA causes episodic gross hematuria after respiratory infections or persistent microscopic hematuria. It is the most common primary glomerulonephritis worldwide.

An acute nephritic syndrome one to three weeks after group A streptococcal pharyngitis or impetigo, with hematuria, hypertension, edema, and low complement C3.

Thrombotic microangiopathy causing microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury; Shiga toxin-producing E. coli is the usual childhood trigger.

Calculated from urine and serum sodium and creatinine to estimate renal sodium avidity. Low values suggest prerenal physiology, but diuretics and neonatal immaturity make interpretation unreliable.

Non-anion-gap metabolic acidosis caused by impaired renal bicarbonate reabsorption or acid excretion. It is classified as distal, proximal, or hyperkalemic and can impair growth.

Proximal tubular dysfunction causing glycosuria, generalized aminoaciduria, phosphaturia, and proximal renal tubular acidosis. Children may present with rickets, polyuria, and growth failure.

Failure of the collecting duct to respond to antidiuretic hormone, producing polyuria and dilute urine. Congenital forms are often X-linked and require free water intake to prevent hypernatremia.

Euvolemic hyponatremia with inappropriately concentrated urine and high urine sodium due to excess antidiuretic hormone activity. Thyroid and adrenal disease must be excluded first.

Serum potassium above the age-appropriate limit. It can cause fatal arrhythmia, so treatment depends on ECG findings, kidney function, and continuing potassium load.

Blood pressure at or above the 95th percentile for age, sex, and height on repeated measurements. In children it is often secondary, so renal and renovascular causes are sought.

Portable cuff recordings over 24 hours that detect white-coat and masked hypertension and assess nocturnal dipping. Pediatric thresholds are specific for sex and height.

High blood pressure from renal artery narrowing, often fibromuscular dysplasia or a genetic syndrome. Clues include high renin, an abdominal bruit, and resistance to usual therapy.

Narrowing of the abdominal aorta and its branches, producing upper-extremity hypertension, weak lower-limb pulses, and sometimes intestinal or renal ischemia. It is a cause of severe pediatric hypertension.

An abrupt fall in glomerular filtration rate detected by rising creatinine or falling urine output and staged by KDIGO criteria. Causes are prerenal, intrinsic renal, or postrenal.

A metabolic emergency after rapid cancer cell breakdown, with hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia. It can cause acute kidney injury and arrhythmia.

Muscle breakdown releases myoglobin, which injures tubules and causes pigment nephropathy. Features include dark urine, elevated creatine kinase, hyperkalemia, and acute kidney injury.

Positive cumulative fluid balance that worsens outcomes in acute kidney injury and critical illness. It is quantified as percentage weight gain and managed with diuretics or renal replacement.

Kidney damage or glomerular filtration rate below 60 mL/min/1.73 m² for at least three months. It is staged by GFR category and albuminuria and requires monitoring for complications.

Loss of body protein and fat stores with inflammation in chronic kidney disease, assessed by appetite, weight, and biochemical markers. It contributes to poor growth and mortality.

Recombinant growth hormone used for short stature in children with chronic kidney disease. It improves height velocity when nutrition, acidosis, and mineral metabolism are optimized.

Abnormalities of calcium, phosphate, parathyroid hormone, and vitamin D metabolism in chronic kidney disease that cause bone disease, vascular calcification, and growth impairment.

Dialysis using the peritoneal membrane as a filter, with catheter-delivered dwells of glucose-based solution. It is common in young children and often performed at home overnight.

Infection of peritoneal dialysate presenting with cloudy fluid, abdominal pain, and fever. Diagnosis uses cell count and culture, and treatment is with intraperitoneal antibiotics.

Neurologic symptoms from rapid osmolar shifts during early hemodialysis, including headache, confusion, seizures, and cerebral edema. Slower clearance and limited initial sessions prevent it.

Extracorporeal blood purification through a dialyzer, requiring vascular access. Children often need a central catheter and careful attention to circuit volume and solute shifts.

Tacrolimus or cyclosporine, drugs that block T-cell activation but cause nephrotoxicity, hypertension, and electrolyte disturbances. Blood levels require monitoring to balance rejection and toxicity.

A calcineurin inhibitor used for maintenance immunosuppression in pediatric kidney transplant recipients. Therapeutic drug monitoring reduces both rejection and drug-related nephrotoxicity.

An antimetabolite maintenance immunosuppressant that inhibits lymphocyte proliferation. It causes gastrointestinal upset and marrow suppression and is teratogenic, so pregnancy prevention is essential.

Immune attack on the allograft causing rising creatinine, sometimes with fever, graft tenderness, or oliguria. Types include antibody-mediated and T-cell-mediated rejection and diagnosis usually requires biopsy.

Antibodies against donor HLA that raise the risk of antibody-mediated rejection and graft loss. They are monitored after transplant and used in pretransplant crossmatch assessment.

Polyomavirus reactivation in the transplanted kidney causing tubulointerstitial inflammation and rising creatinine. Treatment mainly reduces immunosuppression to allow immune control.

Retrograde urine flow from the bladder to the ureter, graded I to V. It is associated with urinary tract infection and renal scarring, especially when high grade.

Obstructing membranes in the posterior urethra of boys causing bilateral hydronephrosis, a thick-walled bladder, and risk of kidney failure. Many cases are detected antenatally.

Prenatal dilation of the renal pelvis measured by anteroposterior diameter. Most cases resolve, but severe or persistent dilation requires postnatal imaging and urologic evaluation.

Bilateral collecting-duct dilatation from PKHD1 mutations, presenting in infancy with enlarged kidneys, hypertension, and portal hypertension from congenital hepatic fibrosis.

An autosomal recessive ciliopathy causing corticomedullary cysts, salt wasting, and progressive chronic kidney disease. It may occur with Joubert or Senior-Løken syndrome.

Hereditary type IV collagen defect causing hematuria, progressive kidney failure, sensorineural hearing loss, and ocular abnormalities. Most cases are X-linked.