54  Kidney Failure

Kidney failure in children represents a significant cause of morbidity and mortality, especially in low- and middle-income countries such as Ghana. It may occur acutely, following a transient insult to the kidneys, or chronically, as the final stage of progressive renal disease. Understanding the causes, pathophysiology, clinical features, investigations, and management of kidney failure is critical for all medical students and healthcare providers involved in child health.

54.1 Introduction

Kidney failure refers to the inability of the kidneys to perform their normal regulatory, excretory, and endocrine functions. In children, it can present as acute kidney injury (AKI) or chronic kidney disease (CKD). AKI involves a rapid decline in renal function over hours or days, while CKD involves irreversible deterioration over months or years. The distinction is important because their causes, management, and outcomes differ.

In sub-Saharan Africa, including Ghana, the prevalence of kidney failure is underestimated due to limited diagnostic resources. However, hospital-based data show that AKI is a common complication of severe infections, dehydration, and nephrotoxic exposure in children, while CKD often results from congenital anomalies or glomerular diseases.

54.2 Classification

Kidney failure in children can be classified as:

• Acute Kidney Injury (AKI):
  • Rapid onset (hours to days).
  • Often reversible if recognized and treated promptly.
  • Common causes: dehydration, sepsis, nephrotoxic drugs, malaria, and hemolytic uremic syndrome.
• Chronic Kidney Disease (CKD):
  • Gradual and irreversible loss of kidney function lasting over three months.
  • Often associated with congenital anomalies, reflux nephropathy, or glomerular diseases.
  • May progress to end-stage renal disease (ESRD), requiring dialysis or transplantation.

54.3 Epidemiology

Global data show that kidney failure accounts for approximately 1–3% of paediatric hospital admissions, though regional variations exist. In Ghana and similar settings, AKI is more frequent than CKD, with mortality rates reaching up to 30% due to late presentation and limited access to dialysis. CKD is less common but often underdiagnosed until advanced stages.

54.4 Aetiology

54.4.1 Acute Kidney Injury

1. Pre-renal causes (impaired perfusion)
   • Severe dehydration (e.g., diarrhoeal diseases)
   • Septic shock
   • Congestive heart failure
   • Hemorrhage
2. Intrinsic renal causes
   • Acute glomerulonephritis
   • Hemolytic uremic syndrome
   • Acute tubular necrosis
   • Nephrotoxins (e.g., aminoglycosides, NSAIDs, herbal medicines)
   • Malaria (especially falciparum infection)
3. Post-renal causes (obstruction)
   • Posterior urethral valves
   • Kidney stones
   • Tumours compressing urinary outflow

54.4.2 Chronic Kidney Disease

1. Congenital anomalies of the kidney and urinary tract (CAKUT)
   • Renal dysplasia
   • Obstructive uropathy
   • Vesicoureteral reflux
2. Glomerular diseases
   • Nephrotic and nephritic syndromes
   • Focal segmental glomerulosclerosis
   • Chronic glomerulonephritis
3. Inherited and metabolic diseases
   • Polycystic kidney disease
   • Cystinosis
   • Alport syndrome
4. Systemic diseases
   • Lupus nephritis
   • Sickle cell nephropathy

54.5 Pathophysiology

The kidneys maintain homeostasis through filtration, tubular reabsorption, secretion, and endocrine regulation. In kidney failure, these functions are impaired, leading to:

• Accumulation of waste products: Elevated blood urea nitrogen (BUN) and creatinine.
• Fluid imbalance: Volume overload, edema, and hypertension.
• Electrolyte abnormalities: Hyperkalemia, hyponatremia, and metabolic acidosis.
• Endocrine dysfunction: Reduced erythropoietin production causes anemia; decreased vitamin D activation leads to hypocalcemia and bone disease.

In CKD, progressive nephron loss leads to compensatory hyperfiltration in the remaining nephrons, which accelerates further damage, forming a vicious cycle that leads to end-stage disease.

54.6 Clinical Features

54.6.1 Acute Kidney Injury

• Oliguria or anuria
• Peripheral or generalised oedema
• Vomiting, lethargy, and poor feeding
• Hypertension
• Pallor (from anemia)
• Seizures due to uremic encephalopathy or electrolyte imbalance

54.6.2 Chronic Kidney Disease

• Growth retardation
• Persistent pallor and fatigue
• Polyuria and nocturia
• Bone deformities (renal osteodystrophy)
• Pruritus, anorexia, nausea, or vomiting
• Late-stage uremic symptoms: confusion, pericarditis, and bleeding tendency

54.7 Investigations

1. Basic Laboratory Tests
   • Serum creatinine, urea, electrolytes (Na⁺, K⁺, Cl⁻, HCO₃⁻)
   • Urinalysis (proteinuria, hematuria, specific gravity)
   • Urine output monitoring
   • Full blood count (for anemia and infection)
2. Special Tests
   • Renal ultrasound: kidney size, echogenicity, and obstruction
   • Renal biopsy (for glomerular diseases)
   • 24-hour urine protein estimation
   • Serum calcium, phosphate, alkaline phosphatase, and parathyroid hormone in CKD
3. Imaging
   • Voiding cystourethrogram (VCUG) for reflux nephropathy
   • DMSA or MAG3 scans for renal scarring or differential function

54.8 Management

54.8.1 Emergency Management (AKI)

• Stabilization:
  • Secure airway, breathing, and circulation.
  • Correct fluid deficits cautiously to avoid overload.
  • Treat underlying causes: antibiotics for sepsis, antimalarials, or stop nephrotoxic drugs.
• Monitor urine output with a catheter.
• Manage complications:
  • Hyperkalemia: calcium gluconate, insulin with glucose, and sodium bicarbonate.
  • Hypertension: diuretics, antihypertensives.
  • Dialysis if unresponsive or in severe uremia.

54.8.2 Ongoing Management (CKD and AKI Recovery)

• Maintain fluid and electrolyte balance.
• Nutritional support, adequate calories and protein.
• Control hypertension using ACE inhibitors or ARBs.
• Manage anaemia with erythropoietin and iron supplements.
• Prevent bone disease with phosphate binders and vitamin D analogues.

54.8.3 Renal Replacement Therapy

Indications include:

• Persistent hyperkalemia
• Severe metabolic acidosis
• Fluid overload unresponsive to diuretics
• Uremic complications (encephalopathy, pericarditis) Modalities:
• Peritoneal dialysis (preferred in infants and young children)
• Hemodialysis - Kidney transplantation (definitive for ESRD)

54.8.4 Preparation for Discharge

• Educate caregivers on dietary and medication adherence.
• Schedule follow-up with a paediatric nephrologist.
• Screen for underlying or recurrent causes.

54.8.5 Long-Term Management

• Regular monitoring of growth, blood pressure, and kidney function.
• Early management of infections.
• Psychosocial support for the child and family.
• Planning for eventual renal transplantation.

54.9 Complications

• Electrolyte disturbances (hyperkalemia, acidosis)
• Hypertension
• Chronic anemia
• Growth failure
• Bone deformities
• Cardiovascular disease (secondary to uremia)
• Infections due to immunosuppression
• Progression to ESRD

54.10 Prevention

• Prompt treatment of infections such as malaria and urinary tract infections.
• Avoidance of nephrotoxic drugs.
• Good hydration during illness.
• Early detection and referral of congenital renal anomalies.
• Regular follow-up for children with known renal disease.

54.11 Prognosis

The outcome depends on the underlying cause, promptness of treatment, and availability of renal replacement therapy.

• AKI has a good prognosis if managed early, though severe cases may progress to CKD.

• CKD often progresses to ESRD without timely intervention.
  Access to dialysis and transplantation markedly improves survival and quality of life.

54.12 Conclusion

Kidney failure in children is a major clinical problem requiring early recognition and multidisciplinary management. In resource-limited settings like Ghana, prevention through early diagnosis and community awareness remains the most effective strategy. Improving access to dialysis and transplant facilities is essential for long-term survival and better quality of life for affected children.