Notes on Questions: Uworld:

Urethral constriction increases the hydrostatic pressure proximal to the constriction, the
pressure increase is transmitted back to the bowmans space increasing the bowman space
hydrostatic pressure and decreasing the GFR
Flow = Pressure/Resistance
RBF = (renal artery pressure renal vein pressure)/renal vascular resistance
RBF = RPF/(1-Hct)
RBF = PAH Clearance/(1-Hct)
PAH uses carrier mediated organic acid transport
DKA = polyuria, polydipsia, and fruity odor to the urine/breath; Lab findings of hyperglycemia
and high anion gap metabolic acidosis with compensatory respiratory alkalosis
DKA is accompanied by hyperpnea (Kussmaul respirations)
Winters formula = PaCO2 = 1.5 (HCO3-)+8 +/- 2
PaCO2 > predicted concurrent respiratory acidosis (when steady state PaCO2 persists above
the range given by Winters formula respiratory failure)
PaCO2 < predicted concurrent respiratory alkalosis
Minimum urinary pH is 4.5
If a patient has an acidosis, then his kidney will excrete H+ and reabsorb the bicarb (see uworld
q.5)
In a normally health individual 55% of the filtered load of urea will be excreted
Acute salicylate intoxication:
-respiratory alkalosis is the first disturbance. Starts soon after ingestion. Salicylates stimulate
medullary respiratory center leading to hyperventaliation, increased loss of CO2, respiratory
alkalosis (low PaCO2)
-few hours later anion gap metabolic acidosis due to accumulation of organic acids in the
blood. After hours, effects of metabolic acidosis become more and more predominant
PaCO2 is less than estimated by winters formula indicating concurrent respiratory alkalosis
Absence of ADH = urine is most hypertonic at the junction between the descending and
ascending limbs of the loop of henle
Presence of ADH = urine is most hypertonic at the end of the collecting ducts
Absence of ADH = urine is most hypotonic at the DCT/Collecting duct
Presence of ADH = urine is most hypotonic at the DCT
Macula densa of the JGA is located at the junction of the ascending loop and distal tubule
Vasopressin produces V2 receptor mediated increase in permeability to water and urea at the
luminal membrane of the inner medullary collecting ducts (MCD)
Vasopressin remember affects only water and urea. So if you are asked a question regarding
vasopressin think of those two things first before thinking of anything else
FE of Creatinine is 110%
Calcium: 50-60% reabsorption occurs at the PCT via the PT paracellular pathway
DT reabsorption of calcium depends on increases in PTH
More than 60% of the fluid reabsorbed even in dehydration occurs in the PCT
Dehydration leads to increased plamsa osmolarity stimulation of osmoreceptors in the
anterior hypothalamus ADH synthesis in the supraoptic nuclei delivered to posterior
pituitary for release
Maximum urine concentrating ability is 1200 mOsm/L
Even at maximum efficiency the kidneys must produce 0.5 L / day to eliminate metabolic wastes
ADH increase permeability of the late distal tubule and CD increasing water reabsorption
approximately 20% of the original filtered volume of free water can reabsorbed here
V1 receptor stimulation leads to vasoconstriction and prostaglandin release

The cortical segment of the CD has mild sensitivity to ADH

The cortical segment of the CD is largely affected by aldosterone
ADH acts mostly on the medullary segment of the collecting duct by enhancing water
permeability of the principal cells
Water channels are returned to the cytoplasm by endocytosis
Hyperosmolarity and depletion of ECV secondary secretion of ADH
Calcitriol = active Vitamin D
End state renal disease (ESRD) can cause hypocalcemia via renal retention of phosphate and
decreased active vitamin D. Hypocalcemia and secondary hyperparathyroidism both
contribute to renal osteodysptrophy
Vomiting causes metabolic alkalosis due to net loss of acidic gastric secretions
Aldosterone release is stimulated by RAAS and high serum K+ level
The net number of molecules diffusing across a semipermeable membrane per a second is
proportional to the molecules concentration difference across the membrane, the total
membrane surface area, and the solubility of the substance. Inversely proportional to the
total membrane thickness and molecular weight of the molecule
Loss of renal parenchyma in kidney disease causes decreased renal calcitriol
production
Calcitriol deficiency leads to decreased calcium absorption and increased calcium loss in the
urine (hypocalcemia)
High phosphate and low calcium levels stimulate PTH secretion from the parathyroid glands
Chronic renal failure is a common cause of secondary hyperparathyroidism High PTH,
low calcium, high phosphate, and low calcitriol (typical lab findings)
PTH mobilizes calcium from the bones in an attempt to increase serum calcium levels
Bone resorption causes bone pain and signs of osteopenia and soft tissue calcification on x-ray
Carrier transport is saturated not maximal rate has been reached
PAH secretion into the tubular fluid by the cells of the proximal tubule by a carrier proteinmediated process
PAH secretion can be saturated
PAH filtration cannot be saturated
In general filtration CANNOT be saturated
Over a wide range of blood pressures (100 mm Hg 200 mm Hg) renal plasma flow is
maintained at a constant level by local changes in vascular resistance
When blood pressure drops below a certain point, auto regulatory mechanisms become unable to
maintain RPF
In the setting of severe hypovolemia, efferent arteriole constriction is not able to fully
compensate for hypovolemia induced decrease in RPF and GFR (more decrease in RPF
than in GFR, decrease in GFR, increase in FF)
Bradykinin is a peptide that stimulates pain, vasodilation and increased vascular
permeability
The cortical collecting duct is the primary site of potassium regulation:
Hypokalemic state, collecting duct alpha intercalated cells reabsorb extra potassium via
H+/K+ ATPase
Factors that increase K+ secretion into tubular fluid:
1. high K+ intake
2. Aldosterone: stimulates Na+/K+ pump
3. Alkalosis: potassium is lost in the urine in order to preserve protons (K+ and H+ freely
exchange across the tubular cell membrane)

4. Diuretics (Loop, thiazide) cause increased flow rate through the distal tubule. Increased
potassium loss in setting of high flow through collecting ducts because the fluid here is dilute
The loop of henle is located in the renal medulla (interstitium is hypertonic)
The water permeability of the distal convoluted tublule is low. 5% of water transport in the
nephron
Elevated serum aldosterone: hypertension, hypokalemia and muscle weakness
Primary hyperaldosteronism (Conn syndrome) dysfunction of RAAS causes inappropriate
aldosterone secretion and decrease in renin levels (if plasma renin is high exclude primary
hyperaldosteronism)
Secondary hyperaldosteronism stimulation of RAAS due to chronic intravascular volume
depletion (both aldosterone and renin elevated). Causes for secondary hyperaldosteronism
include renalvascular hypertension (fibromuscular dysplasia or atherosclerosis), diuretic use,
malignant hypertension, and renin secreting tumors (reninomas)
Reninomas are benign; strongly considered in patients with marked hyperreninemia and HTN
who clearly do not have renal artery disease
Black and elderly patients with low renin is typical clue for essential hypertension