renal essay - acute kidney injury Flashcards
What tends to the be the first sign of an acute kidney injury?
Fluid retention
What are the symptoms of uraemia (build up of nitrogenous wastes in the blood) in AKI?
anorexia, nausea/vomiting, seizures, myoclonic jerks, coma
How does urine output change over the course of an AKI?
Initially urine output is maintained due to compensatory mechanisms, but then nephron damage or obstruction causes oliguria. During AKI recovery, there is usually massive polyuria causing electrolyte imbalance.
What are the general principles of management in AKI?
regulate volume and cardiac output, avoid catheterisation to reduce sepsis risk, renal support with dialysis
What is a pre-renal AKI?
Low blood pressure and reduced renal perfusion cause low GFR and damage to tubules of an otherwise healthy kidney
What are some causes of pre-renal AKI?
Hypovolemia, hypotension/shock, low cardiac output, renal artery contriction
What systems will be activated by a drop the initial drop in perfusion in a pre-renal AKI?
Renin-Angiotensin II, aldosterone, ADH, renal sympathetic nerves
What is the process of volume restoration with renin and ang II in response to low renal perfusion?
- renin released from JGA in response to reduced renal perfusion pressure at the afferent arteriole
- renin cleaves angiotensinogen to ang I, and ACE converts Ang I to Ang II
- Ang II contricts the efferent arteriole, reducing filtered load,
- tubular reabsorption of sodium increases, which increases water reabsorption
- vasocontriction occurs in the vasculature of the body, increasing total peripheral resistance and raising BP further.
What is the process through which Aldosterone increases sodium and water retention?
- Ang II triggers the release of aldosterone from the adrenal glands
- Aldosterone acts on Na+/K+ transporters on principal cells of distal tubule, increasing sodium and chloride reabsorption, while increased excretion of K+
- Upregulate sodium channels in the collecting duct, further increasing reabsorption
What is the process through which ADH increases sodium and water retention?
- Ang II acts on the hypothalamus to trigger thirst and ADH release
- ADH acts of the collecting duct and distal tubules, inserting aquaporins to increase water reabsorption
- At high concentrations, ADH will trigger arteriolar vasoconstriction in the periphery to raise BP
What is the process through which renal sympathetic nerves increase sodium and water retention?
- further activate RAAS in response to low volume, by increase the release of renin
- increase sodium reabsorption in the tubules
- increase renal vascular resistance to drop GFR and renal blood flow.
What pathology does renal hypo-perfusion eventually lead to?
Acute Tubular Necrosis
Which parts of the nephron are susceptible to renal hypo-perfusion and acute tubular necrosis, and why?
Late proximal tubules, thick ascending limbs in the medulla, because they have high oxygen demands due to their active transport processes. Vascular endothelium may also be damaged
How does Acute Tubular Necrosis alter urine output?
Necrotic debris/casts will accumulate in the lumen of the distal tubule, impeding urine output and worsening kidney damage.
How does Acute Tubular Necrosis alter electrolyte and acid-base balance?
Damage to the distal tubule causes a metabolic acidosis and hyperkalemia
What is the histological morpholgy in pre-renal AKI?
Normal glomeruli, necrotic tubular epithelial cells, necrotic debris and cell apoptosis
What investigations are used to diagnose a pre-renal AKI?
Lying & standing BP, JVP, body weight, urine biochemistry/output
What are the clinical findings in the early stages of a pre-renal AKI?
postural hypotension, JVP not visible, weight loss, high urine osmolarity/oliguria, low urine sodium (may become elevated in acute tubular necrosis due to distal tubule damage)
What are the principles of management in pre-renal AKI?
Correct underlying hypotension/hypovolemia, correct acid/base abnormalities (dextrose/insulin for hyperkalemia, sodium bicarb for acidosis), dialysis
What is intrarenal AKI?
Intrinsic structural damage to renal structures, most commonl the tubules, that impairs filtration and absorption
What are some of the causes of intrarenal AKI?
glomerulonephritis, vasculopathies, interstitial nephritis, nephrotoxin acute tubular necrosis
What investigations can be used to diagnose an intrarenal AKI?
renal biopsy, toxicology, immunology, urinalysis, biochemistry, ABG
What are the general principles of management of an intrarenal AKI?
Remove/treat source of injury, immunosupressive treatment for immunological pathologies, correcting acid/base and electrolyte/fluid abnormalitie
What is a post-renal AKI?
Injury to the kidney caused by pressure from an obstruction of urine flow in the kidney or urinary tract
What are some of the causes of post-renal AKI?
cell debris/crystals in tubules, strictures, nephrolithliasis, clots, tumors, neurogenic bladder, prostatic hypertrophy
How does urinary obstruction lead to kidney damage and AKI?
Increased intratubular pressure reduces filtration and tubular flow. Back pressure will reduce GFR at the glomerulus
What investigations can be done to diagnose post-renal AKI?
urine output, urine microscopy, ultrasound/abdominal exam/prostate exam, plasma creatinine, eGFR
What are the possible clinical findings in post-renal AKI?
Anuria or oliguria, haematuria, elevated uric acid, tumors/masses/prostatic hypertrophy, pain
What is the most important management consideration immediately following the removal of an obstruction in post-renal AKI?
There will be massive post-obstructive diuresis, which can cause electrolyte abnormalities and volume depletion
How may an MI lead to AKI?
MI may lead to heart failure - which reduces perfusion to the kidneys by reducing cardiac output and blood pressure
How does MI lead to mitral valve dysfunction and therefore a murmur?
MI causes ischaemic damage to the papillary muscles of the mitral valve, leading to mitral regurgitation
How does mitral regurgitation lead to heart failure (both left and right)?
- Regurgitation increases pressure in the left atrium, which results in atrial hypertrophy.
- Increased volume in the left ventricle will cause hypertrophy and eventually dilation and heart failure.
- Back pressure into the lungs causes pulmonary oedema and hypertension.
- Pulmonary hypertension puts strain on the right heart, which hypertrophies and eventually fails too, causing peripheral oedema and a raised JVP.
What is the process through which heart failure causes volume retention (which exacerbates oedema and heart dysfunction)?
heart failure/IHD reduced cardiac output and blood pressure, reducing renal blood flow. the RAAS system is activated by reduced GFR, causing sodium and water retention which increases the preload on the heart, worsening heart function
What are the first line treatments for an AKI caused by heart failure?
Frusemide - removes excess fluid to relieve pulmonary and peripheral oedema.
What are the second line treatments for AKI caused by heart failure, and why?
ACE Inhibitors - promotes systemic vasodilation to reduce preload and work on the heart
Beta-Blockers - decrease heart rate to increase time in diastole and improve coronary perfusion and overall heart functioning
How can ACE inhibitors prevent renal ischaemia?
While they cause a transient decrease in GFR initially by vasodilating the efferent arteriole, they also promote downstream renal perfusion which prevents ischaemia and progression to Acute Tubular Necrosis
