Renal Disorders

Question 1

Renal corpuscle

Answer 1

Glomerular capillary bed and bowman’s capsule

Question 2

Glomerular filtration membrane layers

Answer 2

Negatively charged

Inner capillary endothelium with small filtration slits

Glomerular basement membrane

visceral epithelium with podocytes to adhere to bowman’s capsule

Question 3

Mesangial cells

Answer 3

Function similar to modified smooth muscle to help regulate pressure

Assist in cleaning the area between capillary balls

Question 4

Juxtaglomerular apparatus

Answer 4

located between the glomerulus and distal convoluted tubule of the same nephron

The distal tubule contains the macula densa

Afferent arteriole contains juxtaglomerular cells

Question 5

Calcitriol

Answer 5

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

Question 6

EPO

Answer 6

Produced by the kidneys in response to low O2 levels

Stimulates bone marrow to produce more RBC

Recycles iron from RBC

Question 7

Renin

Answer 7

Released by JGC in response to the macula densa sensing ow Na levels

Stimulates RAAS

Question 8

Myogenic mechanism of renal autoregulation

Answer 8

Increased afferent arteriole pressure leads to stretch, Ca2+ channel opening, vasoconstriction, and decreases GFR

Decreased afferent arteriole pressure leads to relaxation and increased GFR

Question 9

Tubuloglomerular feedback mechanism of renal autoregulation

Answer 9

Macula densa, JGC, and renin

Angiotensin II causes efferent arteriole constriction and an increase in GFR (without impacting RBF)

Question 10

Serum creatinine

Answer 10

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

Question 11

Serum Cr and GFR

Answer 11

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

Question 12

BUN

Answer 12

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

Question 13

BUN:Cr

Answer 13

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

Question 14

GFR

Answer 14

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)

Question 15

Urine pH

Answer 15

Normal: 5-6.5

After eating or sleeping: 4.5-8 (transient)

Question 16

Urine osmolality

Answer 16

Normal: 500-850 mOsm/kg

Question 17

Urine specific gravity

Answer 17

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

Question 18

AKI

Answer 18

A sudden and often reversible decline in kidney function characterized by oliguria, increased serum creatinine, and increased BUN

Question 19

Oliguria parameter in AKI

Answer 19

UOP usually <0.5 ml/kg/hr for at least 6 hours

Question 20

Serum Creatinine parameter in AKI

Answer 20

> /= 0.3 mg/dL within 48 hours

OR

> /= 1.5x’s the baseline of the prior 7 days

Question 21

Prerenal AKI

Answer 21

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

Question 22

Intrarenal

Answer 22

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

Question 23

Nephrotic syndrome

Answer 23

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

Question 24

Nephritic syndrome

Answer 24

Typically caused by attack of the glomerulus by the immune system

Characterized by hematuria with RBC casts, HTN, and sub-nephrotic proteinuria

Question 25

Postrenal AKI

Answer 25

Most rare

Caused by acute urinary tract obstruction

Usually has to affect both kidneys

Dx with diagnostic imaging, not usually labs

Question 26

AKI symptoms

Answer 26

Oliguria
Chest pain
SOB
JVD
Edema
Confusion
N
Seizures
Coma

Question 27

AKI signs

Answer 27

Metabolic acidosis
hyperkalemia
uremia
azotemia

Question 28

AKI stages

Answer 28

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)

Question 29

CKD

Answer 29

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

Question 30

1 cause of CKD

Answer 30

diabetic neuropathy

Question 31

Renal osteodystrophy

Answer 31

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

Question 32

Anemia in CKD

Answer 32

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

Question 33

CKD acid-base alterations

Answer 33

As GFR is reduced, ability concentrate and dilute urine diminishes

Question 34

CKD systemic effects

Answer 34

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