Acute kidney injury lo's Flashcards
Acute kidney injury
Rapid decrease in glomerular filtration that results in abnormal fluid and electrolytes balance and azotemia, increase in serum creatinine abruptly
Cause of acute kidney injury
- pre-renal
- intrinsic
- post-renal
Pre-renal (60%)
- conditions that cause reduced renal perfusion
- hypovolemia (vomiting, diarrhea, sweating, burns, diuretics, dehydration)
- Hypotension (sepsis, cardiogenic shock –> decreased CO, anaphylactic shock
- Decreased circulating volume eg congestive heart failur, cirrhosis, liver failure, abdominal compartment syndrome, nephrotic syndrome, acute pancreatitis
- Renal artery stenosis
- Drugs ( NSAID’s, ACE inhibitors, cyclosporine, tacrolimus)
renal/intrinsic AKI (35%)
- Any condition that leads to severe direct kidney damage
- Acute tubular necrosis (85%)
- Acute interstitial nephritis
- Vascular diseases
- Glomerulonephritis
Post-renal (5%)
- any condition that results in bilateral obstruction of urinary flow from the renal pelvis to the urethra
- benign prostatic hyperplasia
- tumors (bladder, prostate, cervical, metastases)
- stones
- neurogenic bladder
- congenital malformations (posterior urethral valves)
- Iatrogenic (catheter-associated injuries)
Azotemia
- elevation or buildup of nitrogenous products in the blood (BUN)
Creatinine
waste product from wear and tear of muscles
Do patients with unilateral urethral obstruction maintain normal serum creatinine levels?
Yes as long as contralateral kidney remains intact
Acute tubular necrosis and causes
- damage and death of epithelial cells that line tubules
- Ischemia due to prolonged hypotension
- Nephrotoxic drugs eg radiographic contrast agents, aminoglycosides, methotrexate, amphotericin B
- Endogenous toxins eg bence jones protein light chains in MM
glomerulonephritis and causes
- inflammation of glomeruli
- Bacterial endocarditis, HIV, HepB/C, post-streptococcal glomerulonephritis
Acute interstitial nephritis and causes
- inflammation of renal interstitium
- Medication eg antibiotics, phenytoin, interferon, PPI’s, NSAID’s, cyclosporin
- Infection eg candida, legionella spp, streptococcus spp, hepatits C, sarcoidosis, amyloidosis
principal laboratory findings that indicate acute kidney injury
- Urea: increased
- Creatinine: serum creatinine will increase
- Sodium: hyponatemia? due to water overload
- Potassium: hyperkalemia
- Calcium: hypocalcemia due to decreased production of of 1,25 OH vitamin d
- Phosphate: hyperphosphataemia, unable to excrete phosphate
- Bicarbonate: metabolic acidosis
- decrease in urine output
- Normocytic anemia
Pathology of acute tubular necrosis
- necrotic proximal tubular cells fall into tubular lumen –> debris obstructs tubules–> decreased GFR –> activation of RAAS–> increased aldosterone release–> increased reabsorption of Na+, H2O–> increased urine osmolality –> ADH secreted –> increased reabsorption of H20/urea
cytological and histological findings of acute tubular necrosis
- muddy brown granular casts
- epithelial cell casts
- free renal tubular epithelial cells ( due to denudation of the tubular basement membrane)
Management pre-renal failure
- correct pre-renal factors
- correct volume overload
Management intrinsic renal failure
- Consider trial of IV fluids; identify and treat underlying causes that require specific interventions
- discontinue nephrotoxic drugs, treat infection
Management post-renal failure
- Relieve the urinary tract obstruction
- stenting, catheter
Phase of AKI
- onset/initiation: blood flow to kidneys decreases and urine output decreases, hours to days
- Oliguric: Urine output less than 400ml/day. Kidneys stop functioning properly, 1-2 weeks, increases in creatinine and urea
- Diuretic: will happen if damage has stopped and kidneys get more blood flow. Diuresis between 4-5l per day. 1-2 weeks
- Recovery: urine output and GFR normalizes. Months to yeas
Causes acute tubular necrosis
- Toxic: injury occurs directly due to nephrotoxic substances
- Ischemic: injury occurs secondary to decreased blood flow
Indications for initiation of artificial renal support (dialysis)
- Refractory fluid overload
- Electrolyte imbalances
- Acid-base disturbances
- Acute poisoning
- Uremic symptoms
Advice for patients with AKI on discharge
- Avoid nephrotoxic medications and drugs that may have a detrimental effect on glomerular perfusion
- Ensure adequate protein and calories intake
- Educate patients on medication and diet
Pathophysiology of pre-renal AKI
- Decreased blood supply to kidneys (due to hypovolemia, hypotension or renal vasoconstriction) –> failure of renal vascular autoregulation to maintain renal perfusion–> decreased GFR–> activation of renin-angiotensin system–> increased aldosterone release–> increased reabsorption of Na+, H2O–> increased urine osmolality –> secretion of ADH–> increased reabsorption of H20 and urea
- creatinine is still secreted in the proximal tubules so blood BUN: creatinine ratio increases
Pathophysiology of intrinsic AKI
- damage to vascular or tubular component of the nephron–> necrosis or apoptosis of tubular cells–> decreased reabsorption capacity of electrolytes, water and/or urea (depending on location of injury along tubular system)–> increased Na+ and H2O in urine–> decreased urine osmolality
Pathophysiology of post-renal AKI
- bilateral urinary outflow obstruction (eg stones, BPH, neoplasia, congenital abnormalities)–> increased retrograde hydrostatic pressure within renal tubules–> decreased GFR and compression of renal vasculature–> acidosis, fluid overload and increased BUN, Na+ and K+
- normal GFR can be maintained as long as one kidney functions normally
Oliguria
- reduced urine output
Anuria
- absence of urine output
Polyuria
- excessive urination
prognosis of AKI (co-morbidities)
- good prognosis but depends on if other co-morbidities present
- Can happen again
- Can progress to CKD
Effect of NSAID’s on the kidney and how they exacerbate effects of volume depletion
- NSAID induced inhibition of of cyclooxygenase leads to reduced production of PG E2 and I2--> constriction of afferent arteriole
Nutritional advice for patient on dialysis
- high quality protein ( meat, poultry, fish, eggs)
- low sodium
- low phosphorous
- low potassium
- adequate calorie intake
- vitamin supplements
Pathological changes in the kidney on xray (KUB)
- evaluation of radio-opaque renal stones
- tumours
- urinary blockages
- stones
Pathological changes in the kidney on ultrasound
- Best initial test as chap and does not involve radiation
used to assess for hydronephrosis (urinary obstruction) - kidney size
- renal masses
- doppler–> vasculature
Types of renal replacement therapy
- hemodialysis
- hemofiltration
- Peritoneal dialysis
- Transplant
Dialysate
- also called dialysis fluid, dialysis solution or bath, is a solution of pure water, electrolytes and salts, such as bicarbonate and sodium.
- The purpose of dialysate is to pull toxins from the blood into the dialysate.
- The way this works is through a process called diffusion.
hemodialysis and why would use it
Dialysis is based on the diffusion of molecules across a semipermeable membrane, which separates blood on one side and the dialysate on the other
- bed bound, no renal function, co-morbidities
hemofiltration and why would use it
- Hemofiltration is based upon the principles of filtration and convection, (as opposed to diffusion) and mimics the function of the glomerular system
- ICU
- used to treat AKI
peritoneal dialysis and why would use it
catheter is placed directly in into peritoneal cavity
similiar to hemodialysis but utilizes patients own peritoneal membrane as the semipermeable membrane
- can be done at home, highly adherent patient due to potential complications , young, high functioning
Transplant and why would use it
- indicated in end stage renal disease, not therapy for AKI
- greater long term surivival rate and better quality of life than dialysis
Urine studies AKI
- urinalysis
- sodium, urea, creatinine and osmolality–>calculates sodium and urea fractions
- urine sediment microscopy
Excretion fractions
- may help to differentiate prerenal AKI from intrinsic AKI
- fractional excretion of sodium (FENa)
- Fractional excretion of urea (FEUrea).
Ureters
- muscular ducts with narrow lumina that carry urine from kidneys to bladder
passage of ureters
- pass over pelvic brim at bifurcation of common iliac arteries then run along lateral wall of pelvis and enter urinary bladder
Potential sites of obstructions by ureteric stones ( constrictions)
- junction of ureters and renal pelvis
- where ureters cross brim of pelvic inlet
- during passage through wall of urinary bladder
Histology of ureters
- transitional epithelium
- superficial layer has large bulbous cells called umbrella cells
- lamina propria lies under epithelium (collagen and elastic fibers)
- muscularis : inner longitudinal and outer circular in upper ureter 3 layers near bladder (inner longitudinal, middle circular and outer longitudinal)
- adventitia: loose connective tissue with blood vessels, nerves and adipose tissue
Transitional epithelium
- changes shape in response to stretching
- appears cuboidal when relaxed and squamous when stretched
Kidneys position
- retroperitoneal space of posterior abdominal wall
- T11-L3 with right kidney slightly lower due to liver
renal hilum
- vessels, nerves and ureters enter/exit renal sinus through renal hilum
- renal vein is anterior to renal artery which is anterior to renal pelvis
renal sinus
- flattened, funnel-shaped expansion of the superior end of the ureter
renal pelvis
receives two or three major calyces, each of which divides into two or three minor calyces
minor calyx
indented by a renal papilla, the apex of the renal pyramid, from which urine is excreted
renal corpuscle
- capillary endothelial cells, podocytes, mesengial cells
- parietal layer: simple squamous
- visceral layer: stellate epithelial cells called podocytes
Proximal convoluted tubule
- simple cuboidal epithelium
- cells well stained, lots of mitochondria
- has a brush border of microvilli
loop of henle
- thin limbs: simple squamous, few mitochondria
- thick ascending limb: simple cuboidal epithelium, no microvilli
distal convoluted tubule
simple cuboidal epithelium
cells smaller than in PCT and look empty due to lack of brush border
macula densa: columnar epithelium
Collecting system
- principal cells: most adundant, cuboidal to columnar, pale- staining, distinct cell membranes
- intercalated cells: few and scattered, slightly darker staining
Types of nephrons
- cortical
- juxtamedullary
cortical nephron
renal corpuscles located in outer part of cortex, have short loops of Henle, and extends only into the outer medulla
juxtamedullary nephron
1/8 of total nephrons, renal corpuscles occur in proximity to the base of the medullary pyramid, and long loops of henle and long ascending thin segments.
Blood supply of kidney
renal arteries: branch of abdominal aorta
renal veins: drain into inferior vena cava
Lymph drainage of kidney
lateral aortic lymph nodes
Nerve supply kidney
renal sympathetic plexus
Coverings of kidney
- fibrous/renal capsule
- perirenal fate
- renal fascia
- pararenal fat
Kidney level
- right:T12-L3
- left: T11-L2
- hilum at L1
Intraperiotoneal vs retroperitoneal
- Intraperitoneal organs are situated in the intraperitoneal space and lined by the peritoneum
- retroperitoneal organs are situated behind the intraperitoneal space and not lined by the peritoneum
Intraperitoneal organs
stomach
liver
spleen
Retroperitoneal organs
kidneys
adrenal glands
pancreas
