Paediatrics and Infectious Diseases · MU Sofia

29. Acute and chronic renal insufficiency

Covers acute kidney injury and chronic kidney disease in children, starting with the KDIGO definition and a table of prerenal, intrinsic and postrenal causes with urine tests distinguishing them. It then reviews haemolytic uraemic syndrome in its three forms, the management of AKI including hyperkalaemia and dialysis indications, and the CKD staging and Schwartz eGFR formula. The note closes with causes, a table of complications and treatments, transplantation and dialysis, and dental and mouth problems in CKD.

Inside: 3 sections · 3 tables · 16 flashcards · 5 min

Topic 29 of 30 in the MU Sofia syllabus for Paediatrics and Infectious Diseases (Dental Medicine, Year 4). The free AceMed note covers it in 3 sections, about 478 words (5 min of reading), with 16 flashcards.

In this note

  1. Introduction
  2. Acute kidney injury
  3. Chronic kidney disease

Introduction

Acute kidney injury (AKI) is a sudden fall in kidney function over hours to days, often reversible. Chronic kidney disease (CKD) is lasting damage or loss of function for more than 3 months. In children the causes and needs differ from adults: dehydration and HUS lead in AKI, congenital anomalies in CKD, and growth is a central concern.

Acute kidney injury

Definition (KDIGO)

Any of: creatinine up by ≥ 26.5 µmol/L (0.3 mg/dL) within 48 hours; creatinine 1.5 times baseline within 7 days; urine output under 0.5 mL/kg/h for 6 hours. Stages 1–3 by size of the rise or fall in urine output. Remember creatinine depends on muscle mass, so a “normal” adult value can be high for a toddler.

Haemolytic uraemic syndrome (HUS)

A thrombotic microangiopathy and the commonest cause of intrinsic AKI in young children. Triad: microangiopathic haemolytic anaemia (fragmented red cells, high LDH, negative Coombs test), thrombocytopenia and AKI.

  • STEC-HUS (90%): Shiga toxin from E. coli O157 (undercooked beef, unpasteurised milk, petting farms) after bloody diarrhoea. Supportive care, dialysis in about half; no antibiotics or antimotility drugs.
  • Atypical HUS: complement dysregulation, no diarrhoea, relapses; eculizumab or ravulizumab.
  • Pneumococcal HUS: after pneumonia or empyema; Coombs-positive; avoid plasma.

Managing AKI

  1. Treat the cause: rehydrate a dry child; relieve obstruction (catheter); stop nephrotoxins.
  2. Strict fluid balance: when oliguric, give insensible losses (about 400 mL/m² a day) plus urine output; weigh daily.
  3. Hyperkalaemia: ECG; calcium gluconate to protect the heart; shift potassium into cells with nebulised salbutamol or insulin with glucose; remove it (furosemide, binders, dialysis); stop potassium intake.
  4. Correct acidosis, hyponatraemia, hyperphosphataemia and hypocalcaemia; control hypertension; nutrition; adjust drug doses.
  5. Dialysis (peritoneal in infants, haemodialysis or continuous haemofiltration) for refractory hyperkalaemia, acidosis or fluid overload (pulmonary oedema), uraemic symptoms (encephalopathy, pericarditis, bleeding), or to allow nutrition.

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