Renal Flashcards
What is AKI?
Abrupt decline in actual GFR (days to weeks), upset of ECF volume, electrolyte and acid/base homeostasis, accumulation of nitrogenous waste products.
What are the risk factors for AKI?
- CKD
- Other organ failure especially heart failure, liver disease and diabetes
- History of AKI
- Use of nephrotoxic drugs
- Use of iodinated contrast agents in the last week
- Over 65 years
What are the prerenal causes of AKI?
Pre-renal failure (dehydration most common) – blood supply compromised
• Volume depletion (diarrhoea vomiting etc.)
• Heart failure
• Liver Cirrhosis
• Renal artery atherosclerosis
What are the intrinsic renal causes of AKI?
Intrinsic renal failure – damage to glomeruli, renal tubules or interstitium
• Glomerulonephritis
• Acute tubular necrosis – most common cause in clinical practice – Causes: Ischaemia such as shock or sepsis and Nephrotoxins such as aminoglycosides, myoglobin (rhabdomyolysis), radiocontrast agents and lead
• Acute interstitial nephritis
• Intrarenal obstruction such as rhabdomyolysis
• Tumour lysis syndrome
What are the post renal causes of AKI?
Post renal failure – obstruction to drainage of both kidneys or a single working kidney
• Stones, blood clots and tumours
• Benign prostatic hyperplasia
• External compression of ureter
How is sodium dealt with by the kidneys during AKI and as it progresses?
During early stages of AKI pre-renal uraemia will be seen where the kidneys try to hold onto sodium to preserve circulating volume and so renal perfusion. As kidney function deteriorates into acute tubular necrosis the kidney loses this ability causing a frank loss of sodium.
What are the clinical features of AKI?
Usually, asymptomatic
Decreased urine output and extremely concentrated urine
Fluid retention and overload expressing itself as pulmonary and peripheral oedema
Arrhythmias secondary to changes in potassium and acid-base balance
Features of uraemia – nausea, encephalopathy, drowsiness, confusion, seizures
What are the two types of renal tubular acidosis?
Tubular Dysfunction
Renal tubular acidosis – failure of patients to acidify urine in metabolic acidosis.
1. Type 1 or distal RTA – failure to excrete hydrogen ions urine becomes alkaline and blood acidic. Actual problems is failure to reclaim potassium
2. Type 2 RTA or Proximal – affecting proximal tubules resulting in bicarbonate to leak into the urine and so urine becomes alkaline and blood acidic.
How should AKI be diagnosed and investigated?
Urine dipstick
U&Es
USS looking for obstruction
CXR – fluid overload
What are the 3 stages of AKI
Stage 1 - 1.5-1.9 times baseline creatinine over last week or >26ug/l increase within 48 hours or <0.5ml/kg/h urine output for 6-12 hours
Stage 2 - 2-2.9 times baseline creatinine or <0.5ml/kg/h for > 12 hours
Stage 3 - 3 times baseline creatinine or increase in serum creatinine to 354ug/l or reduction in eGFR to <35ml/min or <0.3ml/kg/h for >24 hours or anuria for >12 hours.
What are the diagnostic criteria for AKI?
- Rise in serum creatinine of 26umol/l or greater over 48 hours
- 50% rise in serum creatinine that has occurred within the last 7 days
- Fall in urine output to less than 0.5ml/kg/hour for more than 6 ours in adults and more than 8 hours in children and young people.
- 25% or greater fall in eGFR in children and young people within the past 7 days
How should AKI be managed?
Assess fluid status
Note if completely anuric check for obstruction especially in catheters
Stop any drugs that reduce kidney function e.g. NSAIDs, ACEi, ARBs, diuretics and aminoglycosides. Also stop metformin, lithium, and digoxin due to increased risk of toxicity
Vasoconstriction of afferent arteriole
Cox-2 inhibitors, Cyclosporine A, NSAIDS, Tacrolimus, Iodinated Contrast
Vasodilation of efferent arteriole
ACEI and ARBs (when used expect 10-20% drop of eGFR but no more)
What are the criteria for referral of an AKI patient to a nephrologist?
- Renal transplant
- Vasculitis/glomerulonephritis/tubulointerstitial nephritis/myeloma
- AKI with no known cause
- Inadequate response to treatment
- Complications of AKI
- Stage 3 AKI
- CKD stage 4 or 5
- May require dialysis
What causes calcium and bone problems in CKD?
Vitamin D synthesis usually finished in the kidneys, so CKD causes low Vitamin D. Kidneys also secrete phosphate, so CKD causes high phosphate. High phosphate draws calcium out of the bones causing Osteomalacia whilst low vit D causes low calcium. All this in turns results in secondary hyperparathyroidism – brown tumours due to over activity of osteoclasts, this is also known as osteitis fibrosa cystica
What causes anaemia in CKD?
Most commonly this occurs due to reduced erythropoietin levels causing a normochromic, normocytic anaemia that becomes apparent when GFR drops below 35ml/min. Can also occur due to reduced absorption of iron, anorexia/nausea, blood loss due to capillary fragility and platelet function
What causes CKD?
Chronic glomerulonephritis Chronic pyelonephritis Genetic – PCK, Alport’s Chronic obstruction AKI Hypertension Cardiovascular disease Diabetes Myeloma Vasculitis and lupus
Why does hypertension occur in CKD?
Kidneys detect the low GFR as indicating blood pressure is too low and so attempt to revert this by releasing renin, conserve salt and water and active sympathetic nervous system which all increase blood pressure.
What are the clinical features of CKD?
Itching Fatigue and malaise due to anaemia Weigth loss due to poor appetite Nausea and vomiting Insomnia Muslce cramps Headaches Erectile dysfunction Fluid overload in advanced disease Hypertension
How should CKD be investigated?
FBC and U&Es – GFR and ACR is (albumin creatinine ratio in the urine) is used to diagnose and classify. ACR sample taken as first-pass morning urine specimen.
Parathyroid function, phosphate, and calcium.
USS looking at size of kidneys and for cysts.
Urine Dipstick
Consider Renal biopsy if appropriate
USS looking at size of kidneys and for cysts.
How is CKD classified based on ACR?
A1 – ACR < 3
A2 – ACR 3-30
A3 – ACR > 30
How is CKD classified based on GFR?
G1 – GFR > 90 with some signs of kidney damage on other tests
G2 – GFR 60-90 with some signs of kidney damage
G3a – GFR 45-59 – this is a moderate reduction in kidney function
G3b – GFR 30-44 – this is a moderate reduction in kidney function
G4 – GFR 15-29 – this is severe reduction in kidneys function
G5 – GFR < 15 – established kidney failure dialysis or transplant likely required
When should a CKD patient be referred to a nephrologist?
- eGFR < 30
- eGFR decrease by 25% or 15 or more within 1 year
- ACR >70mg/mmol unless known to be caused by diabetes and already treated
- ACR > 30mg/mmol or more with persistent haematuria after excluding UTI
- Uncontrolled hypertension despite use of at least 4 antihypertensives
- Suspected or confirmed rare or genetic cause of CKD e.g. PCKD
- Suspected renal artery stenosis
How should hypertension be managed in CKD?
Aim for 140 systolic, key to managing proteinuria are ACEi or ARB. As these drugs reduce filtration pressure a small falling GFR should be expected. NICE suggest 25% reduction in GFR or a rise of up to30% creatinine is acceptable. Furosemide also useful, especially when GFR drops below 45ml/min and has the added benefit of lowering serum potassium.
How are lipid levels managed in CKD?
Atorvastatin 20mg should be offered to patients with CKD. Increase the dose of greater than 40% reduction in non-HDL cholesterol not achieved and FR > 30.
How is anaemia managed in CKD?
Target Hb of 100-120g/ml. Check iron levels and correct this first before administering erythropoiesis stimulating agents such as erythropoietin and darbepoetin.
What are the side effects of erythropoietin?
SE of erythropoietin • Accelerated hypertension which can lead to encephalopathy and seizures • Bone aches • Flu-like symptoms • Allergic reaction • Pure red cell aplasia • Raised PCV increases risk of thrombosis • Iron deficiency
How are calcium and phosphate managed in CKD?
Vitamin D replacement (calcitriol) for those that need it. Reduce dietary intake of phosphate and use phosphate binders – calcium based binders can cause hypercalcaemia and vascular calcification, non-calcium based binders such as Sevelamer are becoming more popular which binds dietary phosphate and prevents absorption. Parathyroidectomy may be required in some cases
If a patient becomes acidotic due to CKD how can this be managed?
Oral bicarbonate supplements to manage acidosis
When is renal replacement therapy required in CKD?
This is required in renal failure which is when native renal function declines to a level no Longer adequate to support health. Usually when eGFR 8-10 Ml/Min and there is presence of uraemic symptoms – acidosis, pericarditis, fluid overload and hyperkalaemia.
What is haemodialysis and what are the potential complications?
This is the most common and involves regular filtration of blood via a dialysis machine, usually 3 times a week. 8 weeks prior to starting an arteriovenous fistula must be formed.
Complications • Site infection • Endocarditis • Stenosis at site • Hypotension • Cardiac arrhythmia • Air embolus • Anaphylactic reaction to sterilising agents • Disequilibration syndrome
What is peritoneal dialysis and what are the potential complications?
A different form of dialysis where the filtration takes place in the abdomen. High dextrose solution injected via a permanent catheter into the peritoneal space, this draws out waste products from the blood. The fluid is then drained after 4-8 hours or a machine does it automatically overnight. This is termed Continuous peritoneal dialysis (CAPD) which involves four 2L exchanges a day.
Complications • Peritonitis • Sclerosing peritonitis • Catheter infection • Catheter blockage • Constipation • Fluid retention • Hyperglycaemia • Hernias • Back pain • Malnutrition
How does someone receive a kidney transplant and what are the potential complications?
Renal transplant
Average wait for a new kidney is 3 years although crossmatched friends and family may be able to speed the process up. Extra kidney inserted in the groin and connected up to the external iliac vessels. Life-long immunosuppressants are required following this.
Complications • DVT/PE • Opportunistic infections • Malignancies (particularly lymphoma and skin cancer) • Recurrent of original disease • Urinary tract obstruction • Cardiovascular disease • Graft rejection
What are the two main categories of polycystic kidney disease?
Autosomal dominant is the most common
Autosomal recessive on Chromosome 6 also exists but rarer – high mortality rate
What causes AD PCKD?
usually inherited but can be de novo in 10% of cases
2 main mutations
PCKD1 – chromosome 16 end stage renal failure at around 50 accounts of 85% of cases
PCKD2 – chromosome 4 end stage renal failure at around 70 accounts for 15% of cases
How does PCKD present?
Usually clinically silent unless the cysts become so large they are symptomatic
Hypertension Headaches Abdominal pain Flank pain Haematuria Renal calculi Hepatic involvement such as interlobular fibrosis
What associated symptoms are there with PCKD?
Liver, ovarian and Pancreas Cysts
Berry aneurysms
How is PCKD diagnosed and screened for?
USS scan is the gold standard
Diagnosis by number of cysts which increase in prevalence with age so need higher number of cysts as you age for diagnosis.
Should screen for intracranial aneurysms if less than 65 years and have family history of aneurysms as increased incidence in PCKD
Relatives of affected individuals screened with abdominal USS
US diagnostic criteria
Two cysts unilateral or bilateral at < 30yrs
Two cysts in both kidneys at age 30-59yrs
Four cysts in both kidneys if aged >60yrs
How is PCKD managed?
Selected patients can receive Tolvaptan (vasopressin receptor 2 antagonist) which slows the progression of cyst development and renal insufficiency. Criteria for use:
• CKD stage 2 or 3 at presentation
• Evidence of rapid progression
High fluid intake
Treat BP to 130/80 using ACEi, thiazide like diuretics and Beta blockers (do not use calcium channel blockers)
Dialysis or transplant
What is Rhabdomyolysis?
Breakdown of skeletal muscle causes toxic levels of myoglobin in the blood which is filtered by the kidney where it causes obstruction and inflammation.
What are the common causes of Rhabdomyolysis?
Crush injuries Strenuous exercise Medications Drug abuse Fall with long lie Epileptic seizures Drugs: Ecstasy and statins (especially when co prescribed with clarithromycin)
What are the clinical features of Rhabdomyolysis?
AKI and disproportionately high creatinine
Raised CK
Myoglobinuria (Light brown coloured urine)
Confusion due to hypocalcaemia (myoglobin binds to calcium)
Elevated phosphate (released from myocytes)
Hyperkalaemia
Metabolic acidosis
How should Rhabdomyolysis be investigated?
U&Es including calcium
Creatine kinase and LDH
MSU
How is rhabdomyolysis managed?
IV fluids
Urinary alkalisation
Dialysis
