Renal Flashcards
Normal arterial blood gas ranges
pH= 7.35-7.45
pCO2= 35-45
pO2>90
HCO3= 22-28
RTA1: distal, pH>5.5
Defective alpha-intercalated cells unable to secrete acid; new bicarb is not generated
this pump normally takes in protons and secretes potassium
metabolic acidosis
hypokalemia
high urine pH
increased risk for calcium phosphate kidney stones due to increased urine pH and increased bone turnover
Causes: amphotericin B analgesic nephropathy multiple myeloma light chains congenital anomalies of the urinary tract
RTA2: distal, pH<5.5
Defect in proximal tubule, bicarb is not reabsorbed, resulting in increased excretion of bicarb in the urine with subsequent metabolic acidosis. Urine is acidified by alpha- intercalated cells in the collecting tubules.
hypokalemia
hypophosphatemia
low urine pH
hypophosphatemia- increased risk for hypophosphatemic rickets
Causes:
Fanconi syndrome (eg Wilson disease)
chemicals toxic to the proximal tubule (lead, aminoglycosides)
carbonic anhydrase inhibitors
RTA4, hyperkalemic pH<5.5
hypoaldosteronism, aldosterone resistance, or K+ sparing diuretics
- hyperkalemia impairs ammoniagenesis in the proximal tubule
- decreased buffering capacity and decreased proton excretion into the urine
MUDPILES anion gap acidosis
anion gap acidosis Methanol Uremia Diabetic ketoacidosis Propylene glycol Iron tablets of INH Lactic acidosis Ethylene glycol (oxalic acid) Salicylates (late)
HARDASS normal anion gap acidosis
normal anion gap acidosis hyperalimentation addison disease renal tubular acidosis diarrhea acetazolamide spironolactone saline infusion
Respiratory alkalosis
psychogenic hypoxemia (altitude) salicylates cause hyperventilation early on tumor pulmonary embolism (acute hypoxemia)
metabolic alkalosis with respiratory compensation (pCO2> 40):
loop diuretics
vomiting
antacid use
hyperaldosteronism (hypokalemia, hypertension, metabolic alkalosis)
pCO2>40
respiratory alkalosis
Respiratory acidosis
hypoventilation: airway obstruction acute lung disease chronic lung disease opioids, sedatives weak respiratory muscles
Linear pattern of IgG deposition on immunofluorescence
Goodpasture anti-glomerular basement membrane antibodies
Lumpy bumpy deposits of IgG, IgM, C3 in the mesangium
PSGN
Deposits of IgA in the mesangium
IgA nephropathy (Berger)
Anti-GBM antibodies, hematuria, hemoptysis
Goodpasture
nephritis, deafness, cataracts
Alport
Crescent formation in the glomeruli
rapidly progressive crescentic glomerulonephritis
wire-loop appearance on light microscopy
lupus diffuse proliferative glomerulonephritis
most common nephritic syndrome in children
minimal change disease
most common nephrotic syndrome in adults
focal segmental glomerulonephrosis, most common in AA, hispanics, HIV infected. Also associated with SCD, heroine abuse, massive obesity, interferon treatment, chronid kidney disease
Kimmelstiel- Wilson lesions (nodular glomerulosclerosis)
diabetic glomerulonephropathy
electron microscopy: effacement of epithelial foot processes
minimal change glomerulonephropathy
Nephrotic syndrome associated with hep B
membranous, membranoproliferative
electron microscopy: subendothelial humps and train tracks
membranoproliferative glomerulonephritis
light microscopy: segmental sclerosis and hyalinosis
focal segmental glomerulonephrosis
purpura on back of arms and legs, abdominal pain, IgA nephropathy, intestinal hemorrhage, arthralgia
Henoch Scholein purpura
Apple- green birefringence with Congo- red stain under polarized light
Amyloidosis
Electron microscopy: spiking of the GBM due to electron- dense subepithelial deposits, “spike and dome”
membranous nephropathy
most common in caucasian adults
membranous, which is idiopathic or associated with SLE, solid tumors, antibody to phospholipase A2 receptor
Nephrotic syndrome
3 criteria for diagnosis include >3.5g/day protein in urine
hypoalbuminemia
edema
you may also see hyperlipidemia as the liver’s response to decreased oncotic pressure (for reasons unknown) is to generate lipoprotein particles. At the same time, TG metabolism is impaired.
increased risk of thrombosis, infection
Nodular hyaline deposits in the mesangia of glomeruli, eosinophilic and acellular, dramatically expanded mesangium, capillaries that have lost their prominence
Kimmelstiel- Wilson
Glomerulonephritis plus pulmonary vasculitis
GPA and Goodpasture both have lung and kidney involvement. GPA has upper respiratory involvement (sinuses, soft palate)
