Renal Disorders Flashcards
Exam I
Renal corpuscle
Glomerular capillary bed and bowman’s capsule
Glomerular filtration membrane layers
Negatively charged
Inner capillary endothelium with small filtration slits
Glomerular basement membrane
visceral epithelium with podocytes to adhere to bowman’s capsule
Mesangial cells
Function similar to modified smooth muscle to help regulate pressure
Assist in cleaning the area between capillary balls
Juxtaglomerular apparatus
located between the glomerulus and distal convoluted tubule of the same nephron
The distal tubule contains the macula densa
Afferent arteriole contains juxtaglomerular cells
Calcitriol
PTH releases in response to low Ca2+ levels
Stimulates renal activation of vitamin D to calcitriol (active form)
Calcitriol aids in absorbing Ca2+ and phosphate from the small intestine
EPO
Produced by the kidneys in response to low O2 levels
Stimulates bone marrow to produce more RBC
Recycles iron from RBC
Renin
Released by JGC in response to the macula densa sensing ow Na levels
Stimulates RAAS
Myogenic mechanism of renal autoregulation
Increased afferent arteriole pressure leads to stretch, Ca2+ channel opening, vasoconstriction, and decreases GFR
Decreased afferent arteriole pressure leads to relaxation and increased GFR
Tubuloglomerular feedback mechanism of renal autoregulation
Macula densa, JGC, and renin
Angiotensin II causes efferent arteriole constriction and an increase in GFR (without impacting RBF)
Serum creatinine
Normal value: 0.7-1.2 mg/dL
A waste product of muscle metabolism (endogenous) and ingestion of cooked meat (exogenous)
Filtered by the kidneys at a relatively constant rate, so no changes to the baseline serum creatinine suggest no/minimal change in the GFR
Impacted by muscle mass, supplements, and protein ingestion
Serum Cr and GFR
Changes in serum creatinine and GFR are related inversely, but not proportional
A reduction in GFR is initially compensated by an increase in tubular active transport creatinine secretion, which prevents a marked rise in serum creatinine
Will not recognize an initial decrease in GFR through serum creatinine measurements
This active transport compensation becomes saturated at 1.5-2 mg/dL of serum creatinine, and then a more significant rise in serum creatinine occurs
BUN
Normal value: between 10-20 mg/dL
Urea nitrogen is a byproduct of protein metabolism produced in the liver and filtered by the kidneys
Transports in the blood to kidneys, but is also reabsorbed by the kidneys
Impacted by things that change protein metabolism and dehydration
**the body attempts to retain Na+, but also retains urea
BUN:Cr
High BUN:Cr (>20 mg/dL) may be suggestive of a pre-renal AKI
Low BUN:Cr (<10) may be suggestive of an intrarenal AKI
GFR
Normal value: 90-120 ml/min
(>60 ml/min can be considered adequate if it is known that no kidney injury is present)
The sum of all filtration of plasma by the nephrons in the kidneys
Measured by serum clearance of endogenous or exogenous substances (Creatinine is most commonly used bc it is cheap and readily available)
Urine pH
Normal: 5-6.5
After eating or sleeping: 4.5-8 (transient)
Urine osmolality
Normal: 500-850 mOsm/kg
Urine specific gravity
Normal: 1.1016-1.022
Indicates the kidneys’ ability to concentrate urine and is a good estimate of osmolality/easier to measure
Approximates osmolality by multiplying the last 2 digits of the USG by 36
Consider hydration status
AKI
A sudden and often reversible decline in kidney function characterized by oliguria, increased serum creatinine, and increased BUN
Oliguria parameter in AKI
UOP usually <0.5 ml/kg/hr for at least 6 hours
Serum Creatinine parameter in AKI
> /= 0.3 mg/dL within 48 hours
OR
> /= 1.5x’s the baseline of the prior 7 days
Prerenal AKI
Most common
Caused by things that occur before the kidney (Usually inadequate renal perfusion)
Labs:
Increased BUN:Cr
Increased serum urea and sodium
Decreased fractional excretion of sodium (<1%)
Increased urine osmolality and specific gravity
Intrarenal
Second most common
Caused by disorders directly involving the kidney (renal parenchymal or interstitial tissue)
Commonly caused by acute tubular necrosis due to ischemia or glomerulopathies (nephrotic and nephritis syndromes)
Labs:
Decreased BUN:Cr
Decreased serum urea and sodium
Increased fractional excretion of sodium (>1%)
Decreased urine osmolality and specific gravity
Nephrotic syndrome
Destruction of the filtration membrane and loss of the negative charge
Leads to the excretion of >/= 3.5 g of protein in the urine per day
Also characterized by low serum albumin, edema, hyperlipidemia, decreased vit D levels, hypothyroidism, and sometimes impaired immune function
Ex. diabetic neuropathy
Nephritic syndrome
Typically caused by attack of the glomerulus by the immune system
Characterized by hematuria with RBC casts, HTN, and sub-nephrotic proteinuria
Postrenal AKI
Most rare
Caused by acute urinary tract obstruction
Usually has to affect both kidneys
Dx with diagnostic imaging, not usually labs
AKI symptoms
Oliguria
Chest pain
SOB
JVD
Edema
Confusion
N
Seizures
Coma
AKI signs
Metabolic acidosis
hyperkalemia
uremia
azotemia
AKI stages
Initiating stage (hours-day, maybe no sx)
Oliguric stage (5-15 days, longer = worse outcomes, sx appear)
Diuretic stage (1-2 weeks)
Recovery stage (months-1 year, GFR 70-80% of BL)
CKD
Progressive loss of renal function (usually > 3 months) and associated with systemic disease
Little potential for reversibility but progression can be delayed
Commonly asymptomatic until renal function is <25% of normal
Staged 1-5
Kidney Disease Improving Global Outcomes (KDIGO) guidelines also use GFR and albuminuria to estimate prognosis
Hyperkalemia and metabolic acidosis are important indicators of CKD progression
1 cause of CKD
diabetic neuropathy
Renal osteodystrophy
Skeletal/vascular abnormalities due to issues with Ca2+ and phosphate metabolism
Begins to become problematic when GFR is ~25% of normal
Hypocalcemia and hyperphosphatemia
Decreased conversion of vitamin D to calcitriol and resultant Ca/Phosphate absorption from the intestines
Decreased phosphate excretion (phosphate binds calcium)
Heightened PTH stimulation causes secondary hyperparathyroidism
-Causes calcium release from bone leading to skeletal weakness and vascular calcifications
Anemia in CKD
Normocytic, normochromic anemia, and hypoproliferative anemia
Typical present in almost all patients by stage 5
Caused by decreased EPO production, RBC survival rates, and abnormal iron metabolism from chronic inflammation
CKD acid-base alterations
As GFR is reduced, ability concentrate and dilute urine diminishes
CKD systemic effects
Fractures/skeletal deformities
Bone pain
Pulmonary edema
LV hypertrophy, cardioomyopathy, HTN, dysrhythmias, atherosclerosis, chest pain
Encephalopathy from progressive accumulation of uremic toxins
Anemia
Anorexia, N/V, peptic ulcers, hiccups, GI bleeds, pancreatitis
abnormal pigmentaiton and pruritus
Sexual dysfunction
