Kidney Failure Flashcards
Define AKI
Acute Kidney Injury (AKI) is characterised by an abrupt fall in GFR (Glomerular Filtration Rate), clinically manifested as an abrupt and sustained rise in serum urea and creatinine. AKI is twice as common as the number of haemodialysis patients. Up to 18% of hospital patients have AKI.
AKI is very important to identify as it increases mortality. For example x8 mortality for AKI + pneumonia than for pneumonia alone.
What is the aetiology of AKI?
Can be split into pre-renal, intrinsic and post-renal cases. Most cases tend to be pre-renal and obstructive (post-renal).
Pre-Renal
Pre-renal causes are due to failure of perfusion, which leads to reduced GFR and oliguria. This can be due to:
-
Disordered autoregulation - i.e. the renal vasculature is unable to regulate renal perfusion pressure. This can be due to:
- NSAIDs
- ACEi/ARBs
- Calcineurin inhibitors
- Hypercalcaemia
- Hypovolaemia either due absolute loss of fluid (I.e. haemorrhage, GI or skin losses) or relative loss of plasma fluid secondary to heart failure, cirrhosis, sepsis etc.
Renal
Intra-renal causes are either due to the glomerulus, renal tubule, the interstitium, or vasculature of the nephron.
- Glomerular disease - Glomerulonephritis (inflammation) or thrombosis
- Tubular injury - Acute tubular necrosis (ATN)
- Ischaemic ATN is associated with sepsis, hypotensionand haemorrhage.
- Nephrotoxic ATN is associated with drugs, radiological contrast agents, uric acid crystals, haemoglobinuria and myeloma.
- Interstitial nephritis (usually caused by drugs such as NSAIDs or methicillin)
- Vascular disease - vasculitis, occlusion (embolicor thrombotic), HUS (Haemolytic Uraemic Syndrome) and TTP (Thrombotic Thrombocytopaenic Purpura)
Post-Renal
Obstructive nephropathy presents as AKI relatively frequently. Secondary to:
- Kidney stones
- Tumour (prostate, or BPH, pelvic, bladder)
- Blood clots
- Retroperitoneal fibrosis
What are the clinical features of AKI?
Many patients are asymptomatic during the early stages of AKI, despite nearly non-functioning kidneys (emphasising why it is so important to be familiar with high-risk patients and high-risk situations). These patients usually present with laboratory findings of increased urea and creatinine(which is due to reduced GFR). They also commonly present with oliguria or if serious anuria.
Clinical features of AKI are due to complications including:
- Uraemia - progressive weakness and easy fatigue, loss of appetite due to nausea and vomiting, muscle atrophy, tremors, abnormal mental function.
- Metabolic acidosis (though alkalosis is less common but possible). This is due to reduced GFR, as the kidney normally excretes acid and retains bicarbonate ions at the distal convoluted tubule. This presents as rapid and shallow breathing, confusion, fatigue, headache.
- Hyperkalaemia (due to metabolic acidosis) may present as palpitations and signs of arrythmias.
- Hypovolaemia (as this can be the cause of pre-renal AKI) which may present with signs such as a non-visible JVP, poor skin turgor, decreased blood pressure and tachycardia.
- Hypervolemia which may present as dyspnoea or peripheral oedema.
What is the investigative approach for suspected AKI?
- AKI may be a medical emergency. It is important to escalate to the right level of care. Two questions must be addressed urgently:
- How high is the K+? Hyperkalaemia is very dangerous.
- What is the volume status? Pulmonary oedema can prove lethal.
- Once patient is stabilised, look for a reversible cause:I.e. is it pre-renal (are theresigns of volume depletion, and therefore can you reverse with fluid resuscitation), is it post-renal? (arrange an urgent USS),what is on the drug chart?
- Differentiating true AKI from stable CKD, or even an acute deterioration, is clearly very important. The two most consistently useful discriminations are previous measurements of renal function and an ultrasound (long-standing renal disease leads to loss of renal parenchyma).
What investigations would you order in someone with an AKI and what could they show?
Bloods:
- U&Es- acutely ↑serum creatinine, ↑serum K+ and metabolic acidosis. ↓Ca2+ and ↓phosphates.
- FBC- anaemia is a sign of chronic kidney disease, WCC can point to infection. Eosinophilia may be present in acute intestinal nephritis.
- Coagulation studies- DIC associated with sepsis.
- LFTs: hypalbuminaemia may imply proteinuria and glomerulonephritis.
Urinalysis:
- Dipstickt o test for infection or haematuria and proteinuria is very important.
- Microscopy can be very useful. Urinary castspoint towards glomerulonephritis. Also eosinophils may be present in acute intestinal nephritis.
- Biochemistry while still loved my postgraduate examiners, are of limited value in everyday practice.
Serology:
Some of these may be needed if intrinsic AKI is suspected.
- ANA (Anti-Nuclear Antibodies) are positive in SLE and other autoimmune disorders.
- Anti-dsDNA also positive in SLE (more specific).
- ANCA- Associated with systemic vasculitis and Wegner’s granulomatosis.
- Antiglomerular basement membrane antibodies.
Imaging:
- Perform CXR urgently if patient has tachypnoea or signs of pulmonary oedema.
- Urgent renal ultrasound may show obstruction (dilated renal caylices), and other changes associated with chronic kidney disease.
Histology:
Biopsy required in a minority of cases only.
Describe the management of Acute Kidney Injury
- Restore volume status - aiming for euvolaemia withfluids and maybe vasopressors. Careful monitoring in ITU.
- Treat hyperkalaemia (see Potassium Imbalance) and pulmonary oedema (see Pulmonary Oedema).
- Manage acidosis if relevant
- Maintain nutrition
- Institute dialysis if necessary
- Treat the cause if possible.
Define Chronic Kidney Disease (CKD)
CKD is defined as a reduction in kidney function (proteinuria, haematuria or reduction in GFR) lasting ≥ 3 months.
What is the epidemiology of CKD?
CKD is often unrecognised until it progresses to End-Stage Renal Disease (ESRD). It is however very common, and is estimated that 10% of the adult population has CKD.
What are the stages of CKD?
Stages 1 and 2 also need symptoms to be CKD
What is the aetiology of CKD?
- The most common cause is diabetes. It is estimated that one third of diabetes patients will develop nephropathy within 5 to 10 years of diagnosis.
- Hypertension is the second most common cause, accounting for one third of all patients on renal replacement therapy.
- Polycystic Kidney Disease
- Infective or Obstructive
- Glomerulonephritis (which can result in nephrotic and nephritic syndromes such as focal segmental glomerulosclerosis, membranous nephropathy, lupus nephritis, amyloidosis, and rapidly progressive glomerulonephritis)
What are the clinical features of CKD
Patients are often asymptomatic until later stages. Symptoms include:
- Hypertension due to activation of the RAS
- Peripheral oedema
- Pulmonary oedema (usually interstitial pulmonary oedema)
- Clinical features of uraemia including: fatigue, weakness, loss of appetite, headaches; pigmented spots; pruritus; anaemia; asterixis, encephalopathy: seizures, somnolence, coma; peripheral neuropathy: paresthesias; Gastrointestinal symptoms: nausea, vomiting.
- Chronic kidney disease-mineral and bone disorder (CKD-MBD): abnormalities of mineral or bone metabolism in the setting of chronic renal disease. Mostly due to secondary hyperparathyroidism causing renal osteodystrophy or osteitis fibrosa cystica.
Patients may also present with signs of an underlying condition such as arthralgia (due to concomitant autoimmune disorder), enlarged prostate gland (obstructive uropathy), rashes (SLE) etc.
Describe the diagnosis of CKD
- Always assume a decrease of eGFR represents AKI until proven otherwise.* Most patients have diabetes and/or hypertension, or other renal disease.
- It is very important to identify patients with CKD because it is associated with a significantly increased risk of cardiovascular disease.*
High-risk groups should be tested for CKD by looking at:
- Urinalysis to detect haematuria and/or proteinuria. Proteinuria is a marker of chronic kidney damage and has prognostic value in the progression of CKD.
- Microalbuninaemia is a risk factor for the development of progressive CKD.
- eGFR (estimated GFR) is more accurate to look at than the serum creatinine alone. Serum creatinine alone is quite a terrible screening test as has a non-linear relationship with GFR, however, is used by nephrologists to monitor patients.
Blood tests:
- ↑ Creatinine
- Electrolytes: hyperkalaemia, hyperphosphatemia, hypocalcaemia
- Monitor blood pH for metabolic acidosis
- ↓ Calcitriol levels
- ↑ Parathyroid hormone (PTH)
- FBC: Anaemia of chronic kidney disease
A renal ultrasound can help diagnose if kidney atrophy is present, or if renal calculi are present. Further imaging may be indicated e.g. MRI/CT.
A renal biopsy is used to determine the pathological diagnosis of chronic kidney disease in glomerular nephrotic and nephritic syndromes, and in people with diabetes with atypical presentations such as rapidly progressive kidney failure.
Describe the management of CKD
- Dietary management including salt restriction, avoidance of high potassium foods.
- Nephrotoxic substances avoidance (NSAIDs, nicotine sulfonamide antibiotics, aminoglycosides, vancomycin, acyclovir, cisplatin and others)
- Strict blood pressure control is essential to prevent disease progression. This is usually with at-least a ACEi or ARB. Most patients will require 2 or more antihypertensives.
- Cardiovascular disease risk modification through the use of statins.
Patients with end-stage renal disease (stage 5) require renal replacement therapy (dialysis) until a renal transplant is available.
If the patient has anaemia of chronic kidney disease: administer synthetic EPO (epoetin alpha), possibly in conjunction with iron replacement depending on serum ferritin and transferrin values.
If patient has secondary hyperparathyroidism: they may require dietary modification, phosphate-binding drugs, ergocalfierol and maybe active vitamin D analogue.
What are the indications for dialysis?
The main indication for dialysis is end-stage kidney disease (stage 5). Other indications can be remembered with the mnemonic AEIOU:
- Acidosis
- Electrolyte abnormalities (hyperkalaemia)
- Ingestion of toxins
- Overload (fluid)
- Uraemic symptoms
What are the types of haemodialysis?
Haemodialysis can happen either through an arteriovenous fistula (anastomosis of an artery and vein) or through a central venous line such as a Tesio line (two ports, one in and one out).
