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Pathophysiology Chapter 28 - Acute Renal Failure and Chronic Kidney Disease
Terms in this set (39)
Renal Failure pathophysiology
low GFR, Juxtaglomerular cells feel low filtrate, stim RAAS system, inc in Na and water retention by aldosterone. Causes inc in BP =Causes edema.
The more pressure we have in body, the more fluid leaks outside vessels and goes to cells. Low Na also gives us pitting edema.
Renal Failure clinical manifetations
o Urea: uremia and uremic poisoning
o Metabolic acidosis
o Collecting duct can't create bicarbonate, bc kidney not fnx.
o Azotemia (uric acid, ammonia, and creatinine)
Renal Failure treatment
Acute Renal Failure Pathophysiology
o Abrupt reduction in renal function cause accumulation of waste materials in blood (occurs over hours-weeks)
o Potentially reversible (if not completely ischemic)
o Ischemia Nephrotoxin causes inflammation of glomeruli (bec leaky) or affects tubules (sec and reab btw peritubular cap is affected)
o The proteins cells leak from inflamed glomerulus get stuck inside tubules and form casts - clump together - forms obstruction inside tubule. Urine past the obstruction is not good, goes back to Bowman's capsule. Tubule will be obstructed, but build up pressure to Bowman's capsule, kills nephron. Oliguria is bc of dec GFR.
In ________ you see a lot of casts in the urine
how do you measure Acute Renal Failure
o Creatinine clearance aka GFR. Remember CupV.
o Serum creatinine will be high, more than 1mg/dl
Serum creatinine in Acute Renal Failure
will be high, more than 1mg/dl
types of Acute Renal Failure
Intrarenal (Acute Tubular Necrosis ATN)
Prerenal Acute Renal Failure etiology
Extrinsic renal failure: renal artery, aorta, and heart
• Cardiac failure and MI =low CO.
• thrombosis in the renal artery.
• renal artery stenosis (narrowing): caused by AS plaques
• Hemorrhage, dehydration, burns = low blood vol and profusion
Prerenal Acute Renal Failure clinical manifestations
• low GFR =oliguria
• high urine SG and osmolality (solids not reabsorbed
• low urine sodium (low GFR, low filtrate, stim RAAS reabsorb
• water, causing even more conc
• signs of fluid overload
Prolonged Prerenal/Postrenal Acute Renal Failure can cause
intrarenal renal failure
Postrenal Acute Renal Failure etiology
Obstruction within the urinary collecting system distal to the kidney
• Benign Prostatic Hyperplasia
• Prostate Cancer (enlarged prostate compress urethra, bladder and ureter).
• Intra-abdominal Tumors.
• Strictures (narrowing lumen, walls of ureters/urethra come together)
Postrenal Acute Renal Failure pathophysiology
compression blocks normal flow of urine. Ex: if block urethra, urine goes to bladder, then ureter, kidney pelvis, calyx, collecting duct. From collecting duct we have same problem of all that pressure building up to Bowman's capsule - tubular reflux.
Postrenal Acute Renal Failure clinical manifestations
obstruction = elevated pressure in Bowman capsule, low GFR
Tubular Acute Renal Failure: Acute Tubular Necrosis ATN etiology
• Ischemia - so prolonged pre-renal failure can cause us to go to ischemic intrarenal failure.
• Nephrotoxic chemicals
o The urine itself, backflow of the urine. Prolonged post-renal failure creating backflow of urine
o Rx: Antibiotics, Aspirin, Radiographic Contrast Material,
Chemotherapy, Recreational Drugs
Tubular Acute Renal Failure: Acute Tubular Necrosis ATN Clinical manifestations
Depends on ATN stage, 3 stages:
Oliguric stage, Diuretic stage, Recovery
Acute Tubular Necrosis, First 1-2 weeks
o Low urine, so low GFR, hypervolemia, HTN.
o Azotemia, uremia and uremic syndrome.
o K+,H+ not sec in DCT = hyperkalemia & metabolic acidosis
o Might need dialysis if pt is really bad
Acute Tubular Necrosis, Next 1-1.5 weeks. Lasts 2-10 days
o Increased urine volume, tubular dysfunction persists,
o Since diuretic stage, GFR will be high, excreting fluid.. But renal failure, that filtration is useless filtration, it's not proper filtration. So we'll have azotemia and high creatinine. Will also see signs of tubular dysfunction.
o Hypovolemia bc we are peeing out
o Hypokalemia excreting K+ just bc there is excessive fnx, RAAS Na and water, excretes K+
Acute Tubular Necrosis, Lasts up to 12 months
o Gradual normalization of serum creatinine and BUN
o Often results in some degree of renal insufficiency
o The cells are dying, in the 3-4 weeks, probably a lot of cells had a chance to go ischemic. So pt might never have complete funx
Glomerular: Acute Glomerular Nephritis
Acute can transform into chronic to give renal failure. If acute is severe enough to in the acute phase, give us acute renal failure
Interstitial Intrarenal Acute Renal Failure
o Is the parenchyma, the supporting tissue around the nephron
o Allergic Interstitial Nephritis - side effect of some Rx.
o Acute Pyelonephritis
Vascular Intrarenal Acute Renal Failure
pre-renal vs. intrarenal chart: Proteinuria
o Pre/post-renal failure - absent proteinuria, nephrons not yet affected. just see RAAS working to retain Na and other stuff, and the glomerulus is filtering fine.
o Intrarenal - proteinuria, the hematuria
Nephrons damaged, glomeruli bec leaky. also water and Na Retension, and so on, you also see the nephron damaging effects
pre-renal vs. intrarenal chart: Urine Specific Gravity
o Prerenal - higher conc, fluid retention, not going to kidney
o Intrarenal btw lower conc 1.01 - 1.02: filtering, decompensation of the RAAS system - juxtaglomerular cells not working anymore
pre-renal vs. intrarenal chart: Urine Na
o Prerenal - less, retaining it Na more.
o Intrarenal - more, filtering more
pre-renal vs. intrarenal chart: Urinary Sediment
o prerenal - just see a few hyaline casts.
o intrarenal - proteinuria and cells escaping, RBC, WBC casts. We also see tubular epithelial cells - as the nephrons are getting damaged, the walls of tubules bec fragile, and as urine passes by they rip cells off, and they form casts.
pre-renal vs. intrarenal chart: urine osmolarity
o Prerenal - more conc
o Intrarenal - less conc
pre-renal vs. intrarenal chart: BUN: Cr ratio
o Prerenal - more conc
o Intrarenal - less conc
cut off for Chronic Renal Failure
GFR <60 ml/min for 3 months with or without signs of kidney damage
Chronic Renal Failure Pathophysiology
progressive and granule irreversible nephron loss. Bc it's gradual the ischemia can go unnoticed and is irreversible.
Chronic Renal Failure: Risk Factors
• Global health problem often linked to other comorbidities:
• Diabetes mellitus - blood sugar deposit damage the glomeruli - called diabetic nephropathy.
• Hypertension - BP in glomeruli over time = nephron damage
• Recurrent pyelonephritis and glomerulonephritis
• Polycystic kidney disease
Polycystic kidney disease
Chronic Renal Failure: Risk Factor (cysts gig as football)
• Two types:
o Autosomal dom: Adult onset. Survival chances good
o Autosomal rec: Congenital, lower survival rate. cysts are dangerous, not just bc can cause renal failure, is bc cyst can form anywhere in the body, including ovaries, including in brain to cause brain aneurism.
Chronic Renal Failure: Two staging techniques
o Percentage of nephron loss
o Reduction in GFR
Chronic Renal Failure: Percentage of nephron loss stages
o Decreased Renal Reserve: Urine is dec bc there is dec renal fnx. Occurs when <75% of nephron lost, so at least 25% still working fine. Asymptomatic, no azotemia. BUN and creatinine normal
o Renal Insufficiency: Renal failure starts when 75-90% of our nephrons are lost. So less than 25% are working. That's when we start seeing very slight, non-specific signs, polyuria, nocturia, some azotemia.
o End-stage Renal Disease: more than 90% of nephrons are gone. That's when we have all our signs of chronic renal disease.
o Notice how this all starts at 25%. When we take a way a kidney from renal transplant, we only have 50% left.
Chronic Renal Failure: stages
o Stage 1: kidney damage asymptomatic when GFR is >90
o Stage 2: mildly dec GFR when GFR is btw 60-90. At this pt don't have renal failure. To Dx chronic renal failure it's 3 months of GFR <60. So at the first two stages we actually have dec renal reserve, dec renal fnx. Not yet renal failure
o Stage 3: When GFR <60 is when we start having renal failure. GFR: 30-59
o State 4: GFR: 15-29
o Stage 5: GFR: < 15 = ESRD
• Chronic Renal Failure: Complications
o Hypertension and cardiovascular disease (hypervolemia, accelerated atherosclerosis, increased RAAS activity, increased SNS activit)
o Uremic syndrome, azoteia
o Metabolic acidosis (acidic waste product retention; kidneys lose ability to secret H ions and bicarbonate)
o Electrolyte imbalance (K, P and Mg retention in blood)
o Renal osteodystrophy (inc PTH causes altered bone and mineral metabolism; kidneys cannot reabsorb Ca)
o Malnutrition (dec intake due to uremic syndrome, depression, dietary limitations and changes in taste)
o Anemia (lack of erythropoietin)
Chronic Renal Failure: Management Prevention
o Early risk identification: lifestyle modifications and comorbidity treatment
o Maintain fluid volume status and cardiac output
o Avoid and monitor nephrotoxic chemicals
o Avoid and treat infections
Chronic Renal Failure: Management Therapeutic Interventions
o Slow progression of CKD: focus of management until stage 4 or 5
o Primary goals: manage ATN, blood glucose control in diabetics, ACE inhibitor or ARBs to reduce proteinuria, and treatment of hypertension and cardiovascular disease
o Nutritional needs: increased calories, calcium and vitamins
o Restriction of: fluids, phosphorus, K, Na, and protein
o Drug therapy: control hypertension, anemia and some electrolyte imbalances
Drug therapy Chronic Renal Failure
o Control HTN w/ ACE inhibitor and ARBs
o For anemia give iron and vitaminB12, and erythropoietin (EPO).
o If we have acidotic pt give bicarb.
o Treat inf, low mortality and morbidity.
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