Renal Phys and nephron loss

Explain the timeline of nephrogenesis

nephrogenesis ends shortly before birth, but can last up to 3 months after birth for preterm infants

What are some factors that can lead to nephron loss?

mother exposed to certain toxins

genetics

fetal alcohol, steroids, or NSAID exposure

kidney donation

acute and chronic kidney injury

Which renal tubular acidosis type?

H+-ATPase dysfunction

type I (distal RTA)

With renal tubular acidosis type I, what do we expect from the urine, metabolics, potassium levels?

What are some other clinical symptoms to look for?

alkaline urine (because H+ is an acid and is not being secreted)

metabolic acidosis (because acid not secreted = acid retained in body)

hypokalemia (because K+ gets secreted in exchange for sodium in the distal nephron)

others: kidney stones, bone de-mineralization, and growth retardation

Which renal tubular acidosis type?

cannot reabsorb bicarbonate (HCO3-) effectively

Renal Tubular acidosis Type II (proximal RTA)

What is a defect in tubular transport resulting in failure to reabsorb: glucose, amino acids, phosphate, bicarb, uric acid, and K+?

What renal tubular acidosis does it go with and why?

Fanconi syndrome

type II RTA (becuase all of those components are reabsorbed in the proximal tubule, and type II is affecting the proximal tubule

With renal tubular acidosis Type II, what do we expect:

metabolically, with K+, with phosphate, and urine

metabolic acidosis: because bocarb is a base and is being excreted in the urine

hypokalemia: K is lost in urine beause more sodium gets delivered to the distal nephron and stimulates aldosterone which causes K+ secretion

hypophosphatemia

urine: glucosuria and aminoaciduria (think Fanconi)

Which renal tubular acidosis type?

aldosterone deficiency or resistance

renal tubular acidosis type IV

With type IV renal tubular acidosis, what do we expect with:

metabolically

K+

ammonium production

metabolic acidosis: impaired H+ secretion

hyperkalemia: becuase aldosterone plays a role in Na+ reabsorption and K+ secretion

hyperkalemia inhibits ammonium production in the proximal tubule which reduces the kidney’s ability to excrete acid (worsening metabolic acidosis)

What disease is associated with:

addison’s disease, diabetic nephropathy, medications like spironolactone, eplerenone, amiloride, and triamterene?

Renal tubular acidosis type IV

What disease is associated with muscle weakness and arrythmias and fatigue?

renal tubular acidosis type IV because of the hyperkalemia

What is the autosomal dominant renal tuublar defect?

Liddle

Which renal tubular defect?

Na/K/2Cl transporter; reabosorption defect in the acending loop of Henle

you see:

metabolic _____

____kalemia

____calciuria

Bartter

metabolic alkalosis

hypokalemia

hypercalciuria

Which renal tubular defect?

reabsorption defect in NCC of DT

you see:

metabolic _____

____kalemia

____calciuria

____magnesemia

Gitelman

metabolic alkalosis

hypokalemia

hypocalcemia

hypomagnesemia

Which renal tubular defect?

GOF mutation, decreased Na channel degredation → increased Na reabsorption

you see:

metabolic _____

____kalemia

_____tension

_____ aldosterone

Liddle

metabolic alkalosis

hypokalemia

hypertension

decreased aldosterone

Which renal tubular defect?

issue converting cortisol to cortisone becuase hereditary 11B-HSD receptor deficiency

syndrome of apparent mineralcorticoid excess

note: you see metabolic alkalosis, hypokalemia, HTN, and decreased aldosterone just like Liddle

Which renal tubular defect can be associated with licorice?

syndrome of apparent mineralcorticoid excess

What is the difference between a BMP and a CMP?

basic metabolic panel: 8 tests

complete metabolic panel: 14 tests: BMP tests + liver and protein tests