Acute Renal Failure and Chronic Kidney Failure Flashcards
Sudden impairment of kidney function
Leads to retention of nitrogenous waste products called
With or without decrease in UO
Acute Kidney Injury
Azotemia
UO in AKI
Oliguria <400ml/day
Anuria <100ml/day
Increase in Creatinine 0.5mg/dl/day
Increase in BUN 10mg/dl/day over several days
AKI
AKI Creatinine value
Inc 0.5 mg/dl/day
BUN AKI value
Increase 10mg/dl/day over several days
Clinical forms of acute renal failure
Prerenal azotemia
Intrinsic renal azotemia
Postrenal azotemia
AKI epidemiology
Complication of hospital and ICU patients
5% admission
30% ICU
50-70% of all cases of ARF
Most common form
Due to renal hypoperfusion without compromising the integrity of renal parenchyma
ECF depletion as in hemorrhage or dehydration
Prerenal azotemia
Prerenal AKI
30% of all AKI due to diseases that involve the renal parenchyma Mostly triggered by ischemia (ischemic ARF) nephrotoxin (nephrotoxic ARF) acute tubular necrosis (ATN)
Renal azotemia
Intrinsic Renal AKI
5-10% of all ARF
Diseases that cause urinary tract obstruction
Postrenal azotemia
Postrenal AKI
Most common cause of postrenal azotemia is
Bladder neck obstruction from prostatic disease
BPH
ARF Diagnostic procedures
Laboratory exams
Urinalysis - casts or proteinuria suggests the specific type of ARF
Fractional excretion of sodium (FeNa) - distinguished prerenal azotemia from other typed
Serial measurements of BUN and Crea
Serum potassium, phosphate, calcium, uric acid, creatine kinase levels - can point to etiology of ARF
BUN/Crea ratio in Pre-Renal
> 15
BUN/Crea ratio in Renal
<15
AKI Radiographic findings
UTZ - useful to exclude obstructive uropathy
CT Scan and MRI - alternative
Pyelography/IVP - to locate obstruction in the urinary tract
Plain film of abdomen can detect nephrolothiasis
Doppler UTZ, MRI, renal angiography
Renal biopsy - for cases where prerenal and postrenal failures are excluded and the cause of intrinsic renal azotemia is still unclear
Encompasses a spectrum of different pathophysiologic processes associated with abnormal kidney function and a progressive decline in GFR
Most last >3 months
Irreversible
Small shrunken kidneys
Chronic Kidney Disease
CKD Stage 1
90 ml/min per 1.73m2
CKD Stages 2,3,4 GFR
60-89 ml/min per 1.73m2
30-59 ml/min per 1.73m2
15-29 ml/min per 1.73m2
CKD RF
Hypertension Diabetes Autoimmune Age African ancestry Family history
Stage of CKD where anemia is prominent
Stage 3 (30-59 ml/kg/min)
CKD Etiology and Epidemiology
Diabetic glomerular disease
Glomerulonephritis
Hypertensive nephropathy (Primary glomerulopathy with hypertension, Vascular and ischemic renal disease)
Autosominal dominant polycystic kidney disease
Other cystic and tubulointerstitial nephropathy
Bone manifestations of CKD
High bone turnover - increased PTH
Low bone turnover - decreased or normal PTH level
PTH reabsorbs calcium at PCT, ALOH (physiologic) additionl at DCT and CD
PTH blocks reabsorption of phosphate in PCT
Reduction of phosphate ions result in a more ionized Ca in blood due to lack of phosphate ion-calcium salt formation (insoluble) dec plasma calcium.
Cardiovascular manifestation of CKD
Vascular calcification
HTN
Heart failure
Pericarditis
Calcemic uremic arteriolopathy
Calciphylaxis
Anemia in CKD
Normocytic normochromic anemia
Stage 3
Decreased EPO
Neurologic abnormalities in CKD are from
retained nitrogenous metabolites
Evident in Stage 3
Early signs include: disturbance in memory, concentration and sleep
Neuromuscular irritability
Periphera neuropathy (Stage 4)
GI manifestations in CKD
Uremic fetor - urine like odor on breath
Gastritis
Peptic disease
Mucosal ulceration
Endocrine metabolic disease in CKD
Glucose metabolism impaired
Decreased estrogen and testosterone
Dermatologic manifestation in CKD
Pruritus
Nephrogenic fibrosing dermopathy
Leading cause of ESRD in US
Major cause of morbidity and mortality from persons with either Type 1 DM or Type 2 DM
Diabetic nephropathy
Edema
Foamy appearance or excessive frothing of urine (proteinuria)
Unintentional weight gain (from fluid accumulation)
Anorexia
Nausea and vomiting
Fatigue
Diabetic nephropathy
24 h urine collection reveals
Microalbuminuria: 150-300 mg/day
Macroalbuminuria: 300 mg/day
N: <150 mg/day
Diabetic nephropathy
Diabetic nephropathy pathologic hallmark
Kimmelsteil-Wilson lesions (glomerular nodular sclerosis)
Thickening of basement membrane
on light microscopy
Diabetic nephropathy Tx
Control hyperglycemia
Optimal therapy for diabetic nephropathy
Strict blood pressure control
Uncontrolled hypertension accelerates the rate of decline of renal function
Adequate control of blood presse <130/80 is recommended
First line therapy for all patients with DM and HTN
Lowers intraglomerular pressure and posses renoprotective properties
Reduces progression from microalbuminuria to macroalbuminuria
Reduces the decline in GFR
ACEI or ARB
Alternative in patients who develop ACE inhibitor associated cough and angioedema
ARB
Cough and angioedema from ACEI use is caused by
bradykinin
Patchy interstitial suppurative inflammation
Intratubular aggregates of neutrophils
Tubular necrosis
Acute Pyelonephritis
Complications Acute Pyelonephritis
Papillary necrosis
Pyonephrosis
Perinephric abscess
Important cause of ESKD in adults and kidney destruction in children with severe lower urinary tract abnormalities
Chronic Pyelonephritis
Forms of chronic pyelonephritis
Reflux nephropathy - most common
Chronic obstructive nephropathy
Xanthogranulomatous pyelonephritis
Most common cause of Pyelonephritis
E coli 75-90%
S saprophyticus 5-15%
Klebsiella 5-10%
Enterococcus
Proteus - staghorn calculi, alkaline urine from urease
Citrobactee
