Acute and Chronic Renal failure Flashcards
Most common causes of ARF in children in the UK:
- Haemolytic Uraemic Syndrome / HUS – low RBC, low platelets and AKI; admit these patients
- Shistocytes on blood film (distorted erythrocytes -> MAHA -> shistocytes)
- Haemorrhagic E. coli O157 (produces shiga toxin) -> infectious diarrhoea
- Acute Tubular Necrosis / ATN – usually in context of organ failure in ITU or after cardiac surgery
Signs and symptoms ARF
Oliguria or anuria
Discoloured urine – brown
Oedema – feet, legs, abdo, weight gain
Fatigue, lethargy, N&V
Pre-renal failure / i.e. hypovolaemia:
* Fluid replacement /circulatory support is key (n.b. little sodium is excreted as the body is trying to maintain it)
Intrinsic renal failure:
* Monitoring water and electrolyte balance
* A high-calorie, normal protein feed will decrease catabolism, uraemia and hyperkalaemia
Post-renal failure:
* Refer immediately to urology if any of the following are present:
* Pyonephrosis
* Obstructed solitary kidney
* Bilateral upper urinary tract obstruction
* Complications of AKI caused by urological obstruction
* Requires assessment of the site of obstruction (i.e. PUV, VUJ obstruction, etc.)
* Relief can be achieved by nephrostomy or bladder catheterisation
Investigaitons of ARF
renal USS (identify obstruction):
CKD = small kidneys
AKI = large, bright kidneys with loss of cortical medullary differentiation
Management of ARF
Diuretics PRN (i.e. to treat fluid overload or oedema whilst the patient is awaiting dialysis)
Fluid restriction
Dialysis – indicated if failure of conservative management, multisystem failure or one of the following:
* Refractory hyperkalaemia
* Refractory fluid overload
* Metabolic acidosis
* Uraemic symptoms (encephalopathy, nausea, pruritis, malaise, pericarditis)
* CKD stage 5 (GFR <15mL/min)
Good prognosis (in childhood) unless masking a more serious condition (e.g. infection following cardiac surgery)
Causes of AKI
This is when there is a sudden, potentially reversible reduction in renal function
Oliguria is usually present (< 0.5ml/kg/hour)
Causes:
NOTE: PRE-renal causes are the MOST COMMON in children
In RENAL failure- casts are often present in the urine, there is salt and water retention; blood protein.
Acute-on-chronic renal failure is suggested by the child having growth failure, anaemia and disordered bone mineralisation (renal osteodystrophy)
AKI Management
USS may be useful to identify obstruction, small kidneys in CKD or large, bright kidneys with loss of cortical medullary differentiation (typical of an acute process)
Use diuretics when necessary e.g. to treat fluid overload or oedema whilst the patient is awaiting renal replacement therapy
Fluid restriction will also be helpful
Consider referral for renal replacement therapy if any of the following are NOT responding to therapy:
* Hyperkalaemia
* Pulmonary oedema and fluid overload
* Acidosis
* Uraemia (e.g. pericarditis, encephalopathy)
PRE-renal failure
* Due to hypovolaemia
* Little Na is excreted because the body is trying to retain it
* Hypovolaemia should be urgently addressed with fluid replacement and circulatory support
RENAL failure
* Monitoring water and electrolyte balance
* A high calorie, normal protein feed will DECREASE catabolism, uraemia and hyperkalaemia
* Emergency management of metabolic abnormalities:
MOST COMMON causes of acute renal failure in children in the UK:
* Haemolytic uraemic syndrome
* Acute tubular necrosis: This usually happens in the context of multisystem failure, in the ITU or following cardiac surgery
NOTE: if causes of renal failure are NOT OBVIOUS, a renal biopsy should be performed to identify rapidly progressive glomerulonephritis- as this needs treatment with immunosuppression
POST-renal failure
* Refer immediately to urology if any of the following are present:
* Pyonephrosis
* Obstructed solitary kidney
* Bilateral upper urinary tract obstruction
* Complications of AKI caused by urological obstruction
* Requires assessment of the site of obstruction
* Relief can be achieved by nephrostomy or bladder catheterisation
Surgery can be performed once fluid volume and electrolyte abnormalities are corrected
ADVICE
Discuss the triggers of AKI such as dehydration and nephrotoxic drugs
Dialysis
Indicated in AKI when there is:
* Failure to conservative management
* Hyperkalaemia
* Severe hyponatraemia or hypernatraemia
* Pulmonary oedema or severe hypertension due to volume overload
* Severe metabolic acidosis
* Multisystem failure
* Peritoneal dialysis or haemodialysis can be undertaken for AKI
* If plasma exchange is part of the treatment e.g. for vasculitis, haemodialysis is used
* If there is cardiac decompensation or hypercatabolism, arteriovenous or venovenous haemofiltration is used as it provides gentle, continuous dialysis and fluid removal.
* AKI in childhood generally has a GOOD prognosis unless it is complicating a more serious condition e.g. severe infection, following cardiac surgery.
Haemolytic Uraemic Syndrome Causes
Characterised by a TRIAD:
1. Acute renal failure (AKI)
2. Microangiopathic haemolytic anaemia
3. Thrombocytopaenia
Typical HUS is secondary to gastrointestinal infection with verocytotoxin-producing E. coli O157:H7
This may be acquired through contact with farm animals or eating undercooked beef
It can also occur with Shigella
It follows a prodrome of bloody diarrhoea
The toxin from these organisms can enter the GI mucosa and localise to the endothelial cells of the kidney, causing intravascular thrombogenesis.
The coagulation cascade is activated
IMPORTANT: clotting is NORMAL in HUS (unlike DIC)
Platelets are consumed and MAHA results from damage to RBCs as they circulate through an occluded microvascular system
Typical diarrhoea-associated HUS has a GOOD prognosis with early supporting therapy (including dialysis)
Atypical HUS has NO diarrhoea prodrome- this may be familial and frequently RELAPSES
- There is high risk of hypertension
- Risk of progressive CKD with a high mortality
Management of HUS
Consult nephrology and haematology specialists
Children with the typical presentation should be hospitalised
Supportive
* Monitor urine output and fluid balance
* Maintain adequate hydration status (avoid cardiopulmonary overload)
* Monitor blood pressure (treat if elevated)
* Treatment should be with CCBs- ACEi can reduce renal perfusion
* Avoid antibiotics, anti-diarrhoeals, narcotic opioids and NSAIDs
* 50% of patients will require dialysis in the acute phase
Long-term follow up is necessary because there may be persistent proteinuria and the development of hypertension and progressive CKD with typical HUS
Definition of CKD
CKD is the progressive loss of renal function that can be caused by many conditions
There are FIVE stages:
Causes of CKD
Stage 5 renal failure is much less common in children than in adults
Congenital and familial causes are more common in childhood- e.g. structural malformations and hereditary nephropathies
Causes of CKD:
* Renal dysplasia +/- reflux
* Obstructive uropathy
* Glomerular disease
* Congenital nephrotic syndrome
* Tubulointerstitial diseases
* Renovascular disease
* PKD
* Metabolic
Clinical features of CKD
CLINICAL FEATURES (of stage 4/5 CKD)
- Anorexia and lethargy
- Polydipsia and polyuria
- Faltering growth/ growth failure
- Bony deformities from renal osteodystrophy
- Hypertension
- Acute-on-chronic renal failure (precipitated by infection or dehydration)
- Incidental finding of proteinuria
- Unexplained normochromic, normocytic anaemia
NOTE: many children with CKD will have had their renal disease detected antenatally
Management of CKD
AIM: to prevent symptoms and metabolic abnormalities, allow normal growth and development and preserve residual renal function
Diet
* Anorexia and vomiting are common
* Calorie supplements or NG/ gastrostomy feeding is often necessary to optimise growth
* Protein intake should be sufficient to maintain growth and normal albumin (but prevent the accumulation of toxic metabolic by-products)
Prevention of renal osteodystrophy
* Decreased activation of vitamin D leads to phosphate retention and hypocalcaemia, which in turn leads to secondary hyperparathyroidism and eventually osteitis fibrosa cystica and osteomalacia
* Phosphate retention (by reducing milk), using calcium carbonate as phosphate binder and activated Vitamin D supplements can help
Control of salt and water balance, and acidosis
- Many children will also have obligatory loss of water and salt
- They need salt supplements and lots of water
- Treatment with bicarbonate supplements is needed to prevent acidosis
Acidosis
- Reduce EPO production and circulation of marrow-toxic metabolites leads to anaemia
- Responds well to administration of recombinant human EPO
Hormonal abnormalities
- Growth hormone resistance, characterised by high GH levels but poor growth, is a feature of CKD
- Recombinant human GH is effective in improving growth for up to 5 years of treatment
- Many children with stage 4/5 CKD will have delayed puberty or subnormal pubertal growth spurt
Dialysis and Transplantation
- A minimum weight needs to be reached before a child can have a kidney transplant in order to avoid renal vein thrombosis
- Kidneys from living related donors have a better success rate than deceased donor kidneys
- The donor HLA is matched as far as possible to the recipient’s
- Survival is high for renal transplants
Current immunosuppression is usually achieved using a combination of:
* Tacrolimus
* Mycophenolate mofetil
* Prednisolone
There is increasing use of minimal steroid regimens which improve growth
Ideally, a child will be transplanted before dialysis is required
Peritoneal dialysis is less disruptive to life and can be done at home
* Either done by cycling overnight using a machine (continuous cycling) OR manual exchanges over 24 hours (continuous ambulatory peritoneal dialysis)
Haemodialysis is an alternative that can be done 3-4 times per week in hospital
