Renal Flashcards
What is the mnemonic for the things that cause anion gap metabolic acidosis? Name each fucking thing.
MUDPILES
Methanol (formic acid)
Uremia
Diabetic ketoacidosis
Propylene glycol (in antifreeze)
Iron tablets or Isoniazid
Lactic acidosis
Ethylene glycol –> oxalic acid (also in antifreeze)
Salicylates (late!) - aspirin
What is the mnemonic for the things that cause non-anion gap metabolic acidosis? Name each fucking thing.
HARDASS
Hyperalimentation (IV feeding)
Addison disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
Calculate the filtration fraction in this patient.
Filtration fraction = GFR/RBF
Use creatinine clearance to calculate GFR and PAH clearance to calculate RBF as all PAH that enters the kidneys ends up in the urine (by secretion, but we DGAF about that).
Other than creatinine, ________ can be used to calculate GFR but is not commonly used. Explain why.
Inulin
It is freely filtered and neither secreted nor reabsorbed by tubules.
Describe handling of PAH by kidney tubules. What is it often used to calculate?
PAH is freely filtered and also secreted by an organic anion transporter in the PCT such that all the PAH that reaches the kidneys via renal arteries ends up in the urine. Therefore it’s clearance can calculate renal blood flow.
Place the following substances on their corresponding line on the graph:
- Glucose
- Inulin
- PAH
- Creatinine
- Amino acids
- Bicarbonate
- Na+
- K+
- Cl-
- Urea
Line 1: substances that are freely fitered and secreted or not reabsorbed (concentrations increase as free water is reabsorbed)
- PAH
- Inulin
- Creatinine
Line 2: substances that are freely filtered and poorly reabsorbed (but less so than substances above)
- Urea
- Cl-
Line 3: substances whose concentrations don’t change much as they travel along the nephron
- Na+
- K+
Line 4: substances that are reabsorbed in the proximal tubule
-HCO3-
Line 5: substances that are reabsorbed like hell in the proximal tubule
- Glucose
- Amino acids
Your patient presents with hypertension (180/115), palpitations, and is found to have hypokalemia. Plasma renin levels are low, and an adrenal mass is seen on CT. What is your Dx? How can this be treated medically?
Conn syndrome (hyperaldosteronism) from an aldosterone-secreting tumor. Aldosterone receptor antagonists can be used (eplerenone is preferred due to fewer side effects over spironolactone)
Describe each of the following types of renal tubular acidosis and physiology of each:
Type 1
Type 2
Type IV
Type 1 RTA (aka distal RTA): occurs due to an inability to generate a negative luminal potential in the cortical collecting duct from a defective V-ATPase that pumps H+ into the tubule in the late DCT/CD (as seen in Sjogren’s syndrome) or due to messed up generation of NH3 from glutamine, which ultimately generates bicarbonate for reabsorption.
Type 2 RTA (aka proximal RTA): due to an inability to reabsorb bicarbonate in the PCT or defective carbonic anhydrase, seen in multiple myeloma and Fanconi syndrome.
Type IV RTA: due to aldosterone resistance -> more Na+ in the tubular lumen -> harder for V-ATPase to pump H+ into lumen
At what pH are uric acid stones more likely to precipitate: high or low pH? Where along the nephron is this environment most likely to be encountered?
Uric acid is less soluble in an acidic (low pH) environment. This is most likely to be encountered at the distal nephron (collecting duct) where the v-ATPase pumps protons out and urine is most concentrated and acidic.