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Acute kidney injury (acute renal failure)

-Rapid decline (<2 weeks) in GFR
-Complicates 5% of hospital admissions
-Loss of the Steady state (amt coming in=amout coming out)

Azotemia

-accumulation of nitrogenous waste
(Lab portion)

Uremia

-Clinical syndrome of multiple organ dysfunction caused by retention of uremic toxins and or lack of renal hormones due to renal failure (Build up of waste that cause the organ dysfunction + azotemia)

Anuria

-less than 100 mls/24 hr, no urine output

Oliguria & Nonoliguria

-less than 500 mls/24 hr urine
-greater than 500 mls/24 hr urine

Concentrating and diluting ability

-can have a range of 0.5 (concentrated) to 12L (diluted) urine and not have acute renal failure
-urine outflow is useful but cant be used to define acute renal failure

Serum Creatinin

-produced by muscles at a continuous rate, excreted by urine.
-Rise in serum creatinin useful diagnostic tool since production = excretion

Diagnosis obstruction

1. rule out (post) obstruction w/ultrasound.
2. Rule out pre-renal, low blood flow (loss of fluid), no lab test based on clinician suspicion (thirst, skin elasticity gone, low neck veins, etc)
-give fluid challenge (diagnostic & treatment for pre-renal

Pre-renal

-any problems with blood flow into afferent arteriole before the glomerulus
-Most common cause of AKI-60%
-underperfusion of kidneys
-commonly due to volume loss

Post-Renal

-after glomerulus, tubules, and collecting duct.
-Obstruction (prostate, pregnancy, cancer)
-5-10%

Intra-Renal (Intrinsic)

-Interstital, Glomerular, Tubular
-30-35%

Diagnosis-Urinalysis Intra-renal

1.Intersitial-WBCs/WBC casts (sq box) in interstitial compartment, 1-2+ protein
2. Glomerular-RCBs/RBC cellular casts present in urine, 3-4+ protein, inflam at glomerulus (Rectangle cast)
3. Tubular-Muddy brown granular casts (RBC) 1-2+ protein (Tube shape cast)

Acute Interstitial Nephritis Causes

1. Drugs most common
-antibiotics (PCN, Ceph, sulfonomides, rifampin, NSAIDS)
-other (analgesics, diuretics, dilantin)
2. Infection (usually viral)
-autoimmune (lupus-inflammation)
-biopsy for diagnosis
-lymphocyte, inflam, if untreated ->fibrosis

Acute Glomerulonephritis Immune-Complex (After infection)

-Post infectious, numerous inflammatory cells (leukocytes)
-proliferation of endothelial, mesangial cells, infiltrating cells filling & distending capillary loops
-Protein and blood in urine

Acute Glomerulonephritis Non-immune-complex

-Acute Crescentic GN
-crescent shape fibrin blocking ultra filtrate though bowman's capsule
-Posse immune=no antibodies present
-requires very aggressive treatment
-Protein and blood in urine

Acute Tubular Necrosis (ATN) causes

1. Pre-renal cause low blood flow supply of o2 & nutrients to kidney tubules, insufficient to meet metabolic demands (hypotension, shock, necrosis)
2. Tubule cells are exposed to a toxic agent (IV dye, some drugs)
-Endogenous (produced by body) or exogenous (medications)

Acute Tubular Necrosis (ATN) Range

-Extreme renal injury, with loss of many tubule cells simultaneously. Little or no urine output, loss excretion function
-Less extreme injury, fewer cells dying over a several day period. May produce normal amt of urine, less impairment of excretory function, with decreased ability to regulate serum fluid and electrolytes

ATN pathology

-variable depending on nature of insult
-low o2=decrease ATP
-large amounts of Na+, Ca++, h2o influx
-cell swells and sloughs off basement membrane forming granular cast
-tube shaped brown cast block urine flow
-Filtered fluid leaks back into blood, back psi, wastes recycled azotemia -> Uremia
-attracts inflammatory cells -> fibrosis

ATN clinically

-if Tubular basement membrane intact, tubule cells may regenerate
-if interstitial inflammation results in fibrosis, permanent damage, no regeneration

Dialysis

*Hemodialysis-blood cleaning via machine
*Peritoneal dialysis-stomach, use body's peritoneal membrane as filter

Renal Transplantation ABO antigen

-ABO blood group antigen expressed on endothelial cells and RBC
-pre-formed antibodies against these antigens can cause and immediate (hyper-acute) rejection
-Antibodies interact with endothelial cells induce vascular injury

HLA antigens

-Expressed on most cell membranes and are related to genetic makeup
-Twins have same HLA=good donors
-Pre-transplant screening is done to prevent HLA-barriers but can also use immunosuppressants

3 Types of Rejection

1. Hyperacute rejection
2. Acute rejection - acute cellular (Tcell) or acute antibody mediated rejection (Bcell)
3. Chronic rejection

1. Hyperacute rejection

-pre-formed antibodies are present and attack the transplanted organ immediately
-tissue damage occurs
-clinically, very dramatic, organ becomes ischemic pale and necrosis
-no effective treatment, prevented with cross matching

2. Acute rejecction

-acute refers to histopathology seen not the time course
-usually occurs in 1st 2 weeks
-may occur later if triggered by some event (stop immunosuppressive drugs, increase immune activity due to existing infection)
-Treated with high doses of steroids and antibodies against lymphocytes

Acute Cellular rejection

1. Characterized by cellular infiltrate around the capillaries (tubulitis), insterstitial lymphocytic inflammation
2. Release of tissue toxic cytokines results in cell destruction
-treat with steroids & thyroglobulins

Acute antibody (humoral) mediated rejection

1. Mainly affects vascular endothelial cells, endothelial cell swelling, mononuclear infiltrate
2. Eventually occulusion of the blood vessel (if severe, kidney is toast)
-antibodies seen all over tubules
-treat with antibodies plasmaforesis

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