Block 4: AKI Flashcards
Continuous renal support
- For very haemodynamically unstable patients that are moved to the intensive care department. Normally a gentle type of dialysis
- Continuous venovenous haemodialysis (CVVHD)
- Continuous venovenous haemofiltration (CVVHF)
- Continuous venovenous haemodiafiltration (CVVHDF)
Complications of AKI- concise
- Fluid overload: leg oedema, pulmonary oedema, pleural effusion
- Electrolyte derangement: hyperphosphatemia, hyperkalaemia
- Acid-base balance: metabolic acidosis
- End organ complications of uraemia
- CKD
- End stage renal disease
When to check PSA and causes of raised lactate
Best to check PSA before inserting a catheter
Causes of raised lactate: reduced organ perfusion/sepsis, metformin use
Post obstruction diuresis (POD)
- A polyuric state where lots of salt and water are eliminated after relief of a urinary tract obstruction.
- Generally occurs after relieving bladder outlet obstruction (BOO), bilateral ureteric obstruction, or unilateral ureteric obstruction in a solitary kidney.
- Diuresis resolves once homeostasis is achieved. These patients are at risk of severe dehydration, electrolyte imbalances, hypovolemic shock, and even death if fluid and electrolyte replacement is not initiated. Can cause ongoing AKI
Pulmonary renal syndrome (PRS)
- Diffuse alveolar haemorrhage plus glomerulonephritis often occurring simultaneously.
- Almost always due to an autoimmune disorder.
- Diagnosis by serology tests and sometimes lung and renal biopsy.
- Treatment includes immunosuppression with corticosteroids and cytotoxic drugs
- Not a specific disease but a syndrome that suggests a differential diagnosis
- Causes: Connective tissue disorder (RA, SLE, Progressive systemic sclerosis), Goodpasture’s syndrome, Renal (IgA nephropathy, idiopathic immune complex glomerulonephritis), Systemic vasculitis (Microscopic polyangitis), drugs, heart failure
Goodpasture’s disease
- Diagnosis: anti-GBM antibodies in the blood or kidney
- Targets the collagen on the basement membrane of alveoli and glomeruli
- It is a rare form of vasculitis that affects the small blood vessels in the kidneys and lungs
- Treatment is with plasma exchange with prednisolone and cyclophosphamide
- If treated quickly good recovery, unlikely to relapse though smoking is a trigger
- If patients on dialysis kidney transplantation is possible when anti-GBM antibodies are undetectable
Rhabdomyloysis
Muscle break down, myoglobin enters the blood stream, goes through the kidneys causing coca-cola urine. In muscle breakdown ATP is depleted causing increased calcium and the generation of free oxygen radicals. This damages the myofilament of the muscle causing increases potassium, phosphate, CK, urate and myoglobin which damage the kidneys
Preventing AKI
- Treatment with IV fluids: fluid resuscitation with 0.9% sodium chloride at a rate of 10-15ml/kg/hr to achieve high urinary flow rates (>100ml/hr), with the cautious addition of sodium bicarbonate 1.4% to maintain urinary pH> 6.51.
- Regular monitoring of U&E’s and CK
- Monitor fluid status to avoid overload
Medications in AKI
- Safe to continue: paracetamol, warfarin , statin (not with rhabdomyolysis), asprin, clopidogrel, beta-blockers
- May worsen renal function: NSAID’s, Aminoglycosides, ACEi, ARB’s, diuretics
Features suggesting CKD not AKI
- Bilateral small kidneys: exceptions are autosomal dominal polycystic kidney disease, diabetic nephropathy, amyloidosis, HIV associated nephropathy
- Hypocalcaemia- due to lack of vitamin D
Kidney- medication
- NSAID’s impair renal autoregulation by inhibiting prostaglandin mediated vasodilation of the afferent arteriole Reduced blood supply through the kidney
- ACEi and ARB’s: reduce systemic blood pressure and also vasodilation of the efferent arteriole. This impairs renal autoregulation and reduced glomerular perfusion pressure.
- If you combine ACi and NSAID’s you would have a lack of blood going in and excess blood leaving, starving the glomerulus of blood
Kidney- Metformin
- Associated with increased risk of lactic acidosis in high risk patients
- Review the dose of metformin if eGFR is below <45
- Stop metformin if eGFR is <30
- Prescribe metformin in caution with rapid change in GFR
- Sulfonylurea increases risk of hypoglycaemia with kidney damage, drug is renally cleared
Kidney- Trimethoprim
Increases risk of hyperkalaemia. Interferes with tubular creatinine secretion causing a rise in creatinine levels and may cause a false positive AKI diagnosis.
AKI definition
An acute rise in creatinine or sustained reduced urine output. Causing failure to maintain fluid, electrolyte and acid-base homeostasis.
Kidney function
1) Excrete water soluble waste products of metabolism
2) Control electrolyte balance
3) Control water volume and balance
4) Control the acid/base balance of the blood
5) Control blood pressure: Through water and electrolyte balance And production of renin
6) Needed for the production of active vitamin D
7) Maintaining haemoglobin through the production of erythropoietin
Inner structure of the kidney
- The kidneys lie retroperitoneally: at vertebral level T12-L3, they are 10-12cm in bipolar length
- The kidneys are surrounded by a tough capsule, and an outer cortex and an inner medulla
- Nephrons in the cortex and medulla filter waste products from the blood, forming urine.
- The pyramids of the cortex drain this into the minor calyces.
- 2-3 minor calyces drain into each of the 2-3 major calyces.
- The major calyces drain into the renal pelvis, which empties through the ureters into the bladder.
Blood flow in the kidneys
- Afferent arteriole supplies blood to the glomerulus: some of it is filtered into the Bowmans capsule
- The filtered blood leaves via the efferent arteriole and divides to form the peritubular capillary network
GFR
- Driven by hydrostatic pressure, oncotic pressure and permeability of glomerular basement membrane (podoctes)
- Approximately 130ml/min/1.73min men and120ml/min/1.73min women
- Begins to decline from 26 years
Role of different parts of the nephron
- Proximal tubule: reabsorbs water, sodium , potassium, bicarbonate, glucose, amino acids. Waste products secreted are creatinine and uric acid
- Loop of Henle: concentration gradient is made through sodium reabsorption allowing urine to be concentrated. Loop diuretics act here. Furosemide acts on the ascending limb
- Distal tubule: re-absorbs sodium, Thiazide diuretics act here
- Collecting duct: reabsorbs some sodium, acid secretion is performed by alpha intercalated cells. ADH acts here inserting aquaporins concentrating urine
Endocrine function of the kidneys
- Vitamin D and renal bone disease: secondary hyperparathyroidism occurs early in CKD. In the kidneys Vitamin D is transformed to its biologically active form
- Kidney regulates calcium and phosphate metabolism through Parathyroid hormone (PTH), calcitriol (1,25 dihydroxycholecalciferol) and calcitonin. Disregulation of calcium and phosphate is a common consequence of CKD which can cause mineral bone disease (CKD-MBD)
- EPO: made by kidneys, prompts bone marrow to make RBC. Treat with erythropoietin stimulating agent (ESA’s) to correct anaemia
