Renal Disease Flashcards
What is AKI and how is it’s severity assessed in children?
Rapid rise in creatinine or development of oliguria/anuria. Severity is based on the paediatric RIFLE criteria that looks at magnitude of changes in GFR, urine output and outcome measures.
What are the common causes of AKI in children in the developed world?
Developed countries:
• Secondary to cardiac surgery
• Bone marrow transplantation
• Toxicity (NSAIDs), aminoglycosides, vancomycin, Aciclovir and contrast)
What are the common causes of AKI in the developing world?
Developing world: • Vomiting and Diarrhoea • Glomerulonephritis • Drug induced haemolysis in G6PD • Snake bite • Haemolytic uraemic syndrome • Myoglobinuria
What are the common causes of acute tubular necrosis in children?
Acute tubular necrosis causes: crush injury, burns, dehydration, shock, sepsis and malaria.
How does AKI present in children?
Anuria, not eating or drinking, systemically unwell
Red cell casts on MSU = GN
Labstix on MSU = haemo/myoglobinuria
Chemistry
Raised potassium, creatinine, urea and phosphate
Decreased calcium, sodium and chloride
How should suspected AKI in children be investigated?
MSU Urine output ECG for signs of hyperkalaemia Us and Es and Blood gas Platelets and clotting studies Urine plasma osmolality BP
Abdominal US and AXR
How should AKI be managed in children?
Treat cause promptly
Treat shock and dehydration if good urine/plasma osmalitiy as it will respond well to rehydration. If the ratio is low, try furosemide
If very high blood pressure, then give nitroprusside
Fluid requirement should be worked out by their daily requirement plus rehydration
Monitor for hyperkalaemia
What is haemolytic uraemic syndrome and what causes it?
This is very rare and occurs due to microangiopathic haemolytic anaemia triggered by shiga toxin producing E. coli. It is characterised by a triad to haemolytic anaemia, AKI and thrombocytopenia.
Acquired from food or water contaminated with E. Coli, shigella or campylobacter.
These bacteria release toxins which bind to the glomerular epithelium stimulating apoptosis and clotting. The clots form all over the body resulting in haemolytic anaemia.
How does haemolytic uraemic syndrome present and how should it be investigated?
Schistocytes, burr cells, thrombocytopenia, AKI
95% of cases associated with diarrhoea
Children usually < 3 years and present in summer
Abdominal pain Raised LDH Decreased haptoglobin Colitis Oliguria and haemoglobinuria Nausea and vomiting Fatigue and oedema CNS signs encephalopathy and coma
Investigations
Full blood count: anaemia, thrombocytopaenia, fragmented blood film
U&E: acute kidney injury
Stool culture looking for evidence of STEC infection
PCR of stool culture for Shiga toxins
How is haemolytic uraemic syndrome managed?
Treatment is supportive e.g. Fluids, blood transfusion and dialysis if required,
there is no role for antibiotics, despite the preceding diarrhoeal illness in many patients
The indications for plasma exchange in HUS are complicated. As a general rule plasma exchange is reserved for severe cases of HUS not associated with diarrhoea
Eculizumab (a C5 inhibitor monoclonal antibody) has evidence of greater efficiency than plasma exchange alone in the treatment of adult atypical HUS
What causes chronic renal disease in children?
Congenital Dysplastic kidneys Pyelonephritis Glomerulonephritis Recurrent UTI Reflux nephropathy - damage from posterior urethral valves AKI that causes cortical necrosis
What features do you get from chronic renal disease in children?
Weakness Tiredness and anaemia Vomiting Headaches Restlessness Twitches Raised BP and retinopathy due to that Failure to thrive Seizures and coma
How should suspected chronic kidney disease be investigated?
Must monitor growth
BP, Us and Es, Ca (often decreased) and Phos (often increased)
How is chronic renal disease managed?
Refer to specialists and get dieticians helps
Make sure high protein diet
Vitamins and maybe GH
Acidosis doesn’t need treating if bicarb is > 20mmol/L
What bone manifestations can occur in chronic renal disease in children?
Be wary of renal osteodystrophy – bone malformations due to low Vit D, Ca and high PO.
Treat raised phosphate with calcium binder, should also treat the low Ca with Vitamin D.
Should children with chronic renal disease be given transfusions if their Hb drops?
Keep high threshold for transfusion as this supresses erythropoietin even if Hb is as low as 60. Instead should give erythropoietin SC.
How should hypertensive emergencies be treated in children with chronic renal disease?
Hypertensive emergencies should be treated with Nitroprusside and Labetalol as an alternative. Keep patient away from light.
What causes acute glomerulonephritis?
Acute Glomerulonephritis Occurs as a result of an immune glomerulonephritis in the kidneys.
Common causes include: Preceding Group B strep throat infection IgA nephropathy (1-2 days) HSP Toxins or heavy metals Malignancies Viruses Bacteria e.g. syphilis Renal vein thrombosis Good Pasture’s and ANCA positive vasculitis
How does acute glomerulonephritis present?
Around 7 years
Haematuria and Oliguria
Increased BP and uraemia
Complicated
Hypertensive encephalopathy - restless, drowsy, severe headaches, fits, reduced vision, vomiting and coma
Uraemia - acidosis, twitching, stupor and coma
Cardiac - gallop rhythm, cardiac failure, cardiomegaly and pulmonary oedema
Uncomplicated
Haematuria, oliguria, raised BP, periorbital oedema, fever, GI disturbance and loin pain
What investigations should be considered in a child with suspected acute glomerulonephritis?
FBC, U+E, complement, Anti DNA antibodies for SLE ANCA antibodies if vasculitis suspected Syphilis serology Blood cultures MSU CXR if fluid overload Renal US
How is acute glomerulonephritis managed?
Supportive
Careful fluid management
Treatment of hypertension and infection
Reduction of blood pressure and proteinuria using ACEi and ARBs
Corticosteroids or other immunosupressants if immune mediated
What is post streptococcal glomerulonephritis?
Presents 7-10 days post infection with pharyngitis or impetigo usually streptococcus pyogenes. This causes immune complex deposition IgG, IgM and C3 in the glomeruli. This is different to IgA nephropathy as it occurs 1-2 weeks post infection, has proteinuria and low complement.
How does post streptococcal glomerulonephritis present?
Gross haematuria (cola coloured) Proteinuria, oedema and hypertension Malaise Anorexia Fever and headache Abdominal pain
How should suspected post streptococcal glomerulonephritis be investigated?
MSU - Haematuria, proteins
FBC U+E (raised urea, creatinine)
Confirm recent strep infection
How is post strep glomerulonephritis managed?
Sodium restriction Diuretics Antihypertensives Penicillin orally for 10 days Regular BP Oedema resolves within 2 weeks, haematuria, BP and proteinuria several weeks
Hypertensive crisis give nitroprusside
What are the 3 main causes of nephrotic syndrome in children?
Minimal change (most common) GN associated with allergy and IgE as a result of Hodgkin’s or NSAIDs. Has a good response to steroids
Membranous glomerulonephritis as a result of infections, rheumatoid drugs and malignancy. 1/3 resolve, 1/3 respond 1/3 progress to CKD
Focal Segmental Glomerulonephritis can be idiopathic or secondary to HIV or heroin.
What are the clinical features of nephrotic syndrome?
Oedema, proteinuria, urinary PCR (protein creatinine ratio) > 200, albumin <25 and hypercholesterolaemia Insidious onset oedema starting periorbital then generalised Anorexia GI upset Infections Irritability Ascites Oliguria Hyperlipidaemia
How should suspected nephrotic syndrome be investigated?
MSU - frothy, albuminous +/- casts, reduced sodium (secondary hyperaldosteronism)
Bloods FBC, U+E - reduced albumin, urea and creatinine normal
Renal biopsy if older and very ill
What complications can occur from nephrotic syndrome?
Pneumococcal peritonitis or other spontaneous infections
Increased susceptibility to infections due to complement loss (consider pneumococcal vaccine if >2yrs
Increased risk of VTE due to loss of antithrombin III
Hypocalcaemia as Vit D and binding protein lost
How is nephrotic syndrome managed?
Reduce salt and protein intake
Fluid restriction to 800-1000ml per day
Diuretics if very oedematous
Albumin only if symptomatic hypovolaemia or severe diuretic resistance
Prednisolone for 4 weeks and then wean over 4 months. Can be steroid sensitive, steroid dependant or steroid resistant (SS, SD or SR)
If steroid toxicity and relapsing NS consider cyclophosphamide, if steroid dependant give ciclosporin but note it is nephrotoxic
