10.2 HUS & Kidney Transplant
Key Takeaways
- Classic (typical) HUS follows Shiga toxin–producing E. coli gastroenteritis and presents with the triad of microangiopathic hemolytic anemia, thrombocytopenia, and AKI.
- Never give antibiotics or antimotility agents for suspected STEC diarrhea — they can increase toxin release and worsen HUS risk.
- Atypical HUS is complement-mediated, may lack a diarrheal prodrome, and often needs urgent complement blockade plus supportive renal care.
- After pediatric kidney transplant, watch for delayed graft function, acute rejection, calcineurin-inhibitor nephrotoxicity, surgical complications, and opportunistic infection from immunosuppression.
- Fever, graft tenderness, rising creatinine, hypertension, and oliguria after transplant are rejection/infection alarms until proven otherwise — never dismiss them as "just dehydration."
Hemolytic Uremic Syndrome in the PICU
Hemolytic uremic syndrome (HUS) is a thrombotic microangiopathy that is a leading cause of community-acquired AKI in previously healthy toddlers and preschoolers. The exam expects you to recognize the clinical triad, separate typical from atypical disease, and prioritize supportive care that does not worsen toxin burden.
The Diagnostic Triad
- Microangiopathic hemolytic anemia (MAHA) — falling hemoglobin, schistocytes on smear, elevated LDH, low haptoglobin, rising indirect bilirubin.
- Thrombocytopenia — platelet consumption in microvascular thrombi; bleeding may be mild despite low counts because clotting factors are relatively preserved compared with DIC.
- Acute kidney injury — oliguria, rising creatinine, hypertension, fluid overload, and often hematuria/proteinuria.
Children may also show pallor, petechiae, irritability, abdominal pain, and neurologic changes (seizures, altered mentation) when cerebral microthrombi occur. Pancreatitis and colitis can accompany the gastrointestinal prodrome.
Typical (STEC) HUS
Typical HUS follows infection with Shiga toxin–producing Escherichia coli (STEC), classically O157:H7, after undercooked ground beef, unpasteurized products, or contaminated produce. A diarrheal illness — often bloody — precedes the triad by days. Shiga toxin injures endothelium, triggering platelet-fibrin thrombi that shear red cells and clog glomerular capillaries.
Critical nursing don'ts: do not give empiric antibiotics for suspected STEC colitis solely to "clear the bug," and do not give antimotility agents. Both can increase toxin exposure and have been associated with progression to HUS. Stool Shiga toxin assay or culture guides public-health reporting; blood cultures are for concurrent bacteremia workup, not the primary diagnostic.
Supportive care is the backbone: careful fluid and electrolyte management, transfusion for symptomatic anemia (avoid aiming for adult-high targets that increase viscosity), platelet transfusion only for active bleeding or invasive procedures, blood-pressure control, and early nephrology involvement for dialysis when hyperkalemia, intractable acidosis, uremia, or pulmonary edema dictate. Most typical HUS cases are self-limited regarding the microangiopathy, but renal recovery varies — some children need chronic dialysis or later transplant.
Atypical HUS
Atypical HUS (aHUS) is usually complement dysregulation (genetic or acquired) without a clear diarrheal STEC trigger — though infection, surgery, or pregnancy can unmask it. Presentation can be fulminant with severe hypertension, anuria, and multiorgan microthrombi. Plasma exchange historically bridged care; modern practice centers on complement C5 inhibition (for example eculizumab) plus vaccination considerations for encapsulated organisms because complement blockade raises meningococcal risk. Differentiate aHUS from TTP (more prominent ADAMTS13 deficiency/neurologic dominance in older patients) using labs and hematology consultation — pediatric TTP is uncommon but life-threatening.
| Feature | Typical STEC-HUS | Atypical HUS |
|---|---|---|
| Prodrome | Bloody diarrhea common | Often no diarrhea |
| Trigger | Shiga toxin E. coli | Complement dysregulation |
| Antibiotics | Avoid in STEC colitis | Treat true infection; not the driver |
| Core therapy | Supportive ± dialysis | Complement blockade + support |
| Recurrence | Uncommon after resolution | Higher without specific therapy |
Distinguishing Mimics
DIC shows coagulopathy (prolonged PT/PTT, low fibrinogen, high D-dimer) beyond isolated thrombocytopenia. Sepsis-associated AKI lacks schistocytic MAHA as the dominant story. Malignant hypertension can cause secondary TMA — control BP aggressively. Always rethink the smear, LDH, and platelet trend when "just AKI" looks too hemolytic.
Pediatric Kidney Transplant: ICU Complications
Children receive transplants for CAKUT, FSGS, congenital nephrotic syndromes, and failed prior grafts. Immediate postoperative PICU priorities are graft perfusion, urine output, fluid balance, and immunosuppression safety.
Early Surgical and Vascular Problems
Delayed graft function (dialysis need in the first week) may reflect ischemia-reperfusion injury, especially with deceased-donor kidneys. Sudden oliguria after initial diuresis raises concern for vascular thrombosis of the renal artery or vein, urine leak, or ureteral obstruction — bedside Doppler, surgical exploration, and catheter/stent assessment are time-critical. Hemorrhage at the anastomosis can present with tachycardia, falling hematocrit, and graft-site swelling.
Hypotension and high intra-abdominal pressure threaten the graft; maintain adequate mean arterial pressure per surgical targets and avoid abdominal compartment physiology after large transplants into small recipients (size mismatch).
Rejection and Drug Toxicity
Acute cellular rejection presents days to months out with rising creatinine, hypertension, fever, graft tenderness, and oliguria. Antibody-mediated rejection may show donor-specific antibodies and microvascular injury on biopsy. Escalate steroids or antithymocyte regimens per protocol — the nurse's job is early recognition and protecting lines/access for therapy.
Calcineurin inhibitors (tacrolimus, cyclosporine) cause afferent arteriolar vasoconstriction and a rise in creatinine that can mimic rejection. Trough levels, interaction checks (azole antifungals, macrolides raise levels), and biopsy often separate toxicity from rejection. Sirolimus and MMF add marrow and wound-healing burdens.
Infection Under Immunosuppression
Opportunistic pathogens — CMV, EBV (PTLD risk), BK virus nephropathy, PCP, candidiasis — peak when induction is strongest. Fever in a transplant recipient is never "viral syndrome until proven otherwise" without a structured workup. Prophylaxis (antivirals, PCP prevention) must continue; missed doses are as dangerous as over-immunosuppression.
Fluid, Electrolytes, and Hypertension
Polyuria from a well-perfused graft can cause hypovolemia and electrolyte wasting — replace urine output milliliter-for-milliliter early per protocol. Hypertension is nearly universal; uncontrolled BP damages the new kidney. Hyperkalemia may reflect rejection, obstruction, calcineurin effect, or ACE-inhibitor use.
Family and Adherence Context
Adolescent non-adherence is a leading cause of late graft loss. PICU readmissions for rejection should trigger adherence assessment, pharmacy review, and social work involvement — tested as Synergy-linked clinical judgment even inside a renal chapter.
A 3-year-old develops pallor, petechiae, and oliguria five days after bloody diarrhea. Labs show hemoglobin 6.8 g/dL, platelets 42,000/µL, creatinine 2.1 mg/dL, high LDH, and schistocytes. The triage nurse should anticipate which immediate priority?
A preschooler without a diarrheal prodrome presents with severe hypertension, anuria, schistocytes, and thrombocytopenia. Complement testing is abnormal. Which therapy pathway is most specific for this presentation?
On postoperative day 2 after living-donor kidney transplant, a child who had been making 3 mL/kg/h of urine suddenly becomes nearly anuric with graft-site swelling and a rising creatinine. The nurse's highest concern is: