Renal Diseases and Conditions Flashcards
Hydronephrosis
Obstruction in urinary system distal to the kidney (after the kidney) causes urine to back up and kilate renal pelvis and calices
Chronic hydronephrosis can cause atrophy and scarring of renal parenchyma, and thinning of cortical rim
Membranous nephropathy
Caused by deposition of immune complexes on glomerular basement membrane
May be secondary to lupus or viral infection, but 80-90% of the time is idiopathic
Dark purple regions on histology stain indicate protein deposition
Diabetic nephropathy
Diabetes among most common causes of kidney failure
Thickening of glomerular basement membranes which leak protein because of their altered structure
Mesangial cells deposit fibrous tissue into spherical structures (nodular glomerulosclerosis) called Kimmelstiel-Wilson nodules. Over time, entire glomerulus replaced by scar tissue and is useless.
Renal failure
Functioning nephrons are lost.
Remaining nephrons try to compensate by increasing GFRs, but this increased filtration force shortens the lives of these remaining nephrons and causes worse renal failure
Person looks very sick
ACE inhibitors slow renal failure by decreasing efferent arteriole resistance and reducing filtration pressure and reducing “strain” on glomeruli
Syndrome of inappropriate ADH secretion (SIADH)
ADH is abnormally high
Makes urine hyperosmotic unnecessarily and dilutes blood plasma because no ADH negative feedback
Caused by head injury causing posterior pituitary to secrete too much ADH or lung tumors secreting ADH
Treat with demeclocycline, which inhibits ADH action on principal cells
Can be temporary! ADH increased because of stress, then can be fixed by relaxing
Central diabetes insipidus
Posterior pituitary unable to secrete ADH so low/zero levels of ADH cause inability to concentrate urine and large volume of dilute urine excreted
Plasma osmolarity increases since losing too much water
Treat with synthetic ADH, dDAVP (1-deamino-8-D-arginine vasopressin)
Nephrogenic diabetes insipidus
Kidney unable to respond to ADH because of defect in receptor, G protein, adenylyl cyclase
Water cannot be reabsorbed and large volume of dilute urine secreted
Increased plasma osmolality
However, circulating ADH increased because posterior pituitary responds to increased plasma osmolarity of blood
Treat with thiazide diuretics (see next flashcard for mechanism)
How are thaizide diuretics used to treat nephrogenic diabetes insipidus?
Inhibit NaCl reabsorption in early distal tubule means it can’t dilute urine, so you get more concentrated urine
Because you’re blocking reabsorption of NaCl, you’re getting rid of more salt and your ECF (plasma) will have less volume –> causes decrease in GFR because hydrostatic pressure in glomerular capillaries is decreased –> this increases reabsorption in the PCT because (1) lower GFR means higher percent reabsorption, and (2) higher oncotic pressure in capillaries compared to tubules pulls water in to be reabsorbed.
(Also, thiazides may directly insert AQP2 into collecting duct)
Overall, less water filtered (decreased GFR) and more water reabsorbed in PCT (due to higher relative concentration in capillaries) so urine volume decreased
Water Intoxication (Hyponatremia)
5% reduction in [Na+] causes difficulty concentrating and diffuse headache
Reduction below 120mM causes anorexia, nausea, vomiting
Reduction below 115mM causes confusion, seizures, coma, death
However, if the reduction happened slowly the body has adjusted (regulated volume decrease) and could have no symptoms
Note: if osmolality change is acute and symptoms serious, do aggressive osmolality restoration, but if change is chronic (>48 hours) and minor symptoms, treatment can be deadly
Salt Intoxication (Hypernatremia)
Apathy, somnolence, disorientation, coma, severe thirst, sometimes fever
Note: if osmolality change is acute and symptoms serious, do aggressive osmolality restoration, but if change is chronic (>48 hours) and minor symptoms, treatment can be deadly
Osmotic diuresis (ie Diabetes Mellitus)
More solute (ie glucose) than the PCT can reabsorb, so is dumped out in urine and brings water along with it
K+, Na+, Cl- lost in the urine
Hypovolemic, dry mucous membranes, lethargy
Treat with IV saline then insulin for DM
Edema
When the volume of interstitial fluid exceeds the ability of the lymphatics to return it to the circulation
Lymphatic drainage impaired when lymph nodes surgically removed or irradiated (in malignancy), in filariasis (parasitic infection of the lymph nodes), or during lack of muscular activity
Can be localized (leg) or generalized (in heart failure, renal disease, etc)
Note: ascites = edema in peritoneal cavity
Pitting edema: as long as Pi negative, skin not deformed by finger pressure, but as fluid accumulates, lateral fluid movement decreases and get a pit when you put finger pressure
Diabetic ketoacidosis
Hyperglycemia from uncontrolled diabetes mellitus (usually type I) causes osmotic diuresis
Lack of insulin causes metabolism of free fatty acids which leads to ketoacid buildup, and blood gets acidic –> body tries to compensate with hyperventilation (blow off CO2)
Ketoacids build up so much that kidney can no longer be reabsorbed and metabolized and instead they dissociate and anions (acetoacetate- and b-hydroxybutyrate-) are excreted and leave H+ behind which acidifies blood
Get hypokalemia (osmotic diuresis/vomiting bring water and K+ out of blood too, aldosterone production causes K+ secretion) even though have high K+ in blood (lack of insulin, high plasma osmolality, H/K exchange to correct acidosis)
Normal lab values
pH: 7.38 - 7.42
Pco2: 40
PO2: 101 - (0.43 x age) +/- 4
CO2: 20 - 29
Anion gap: 12 +/- 2
Glucose: 80
BUN: 7 - 23 mg/dL
Creatinine: </= 1.3 mg/dL
BUN/creatinine: </= 15:1 (>20:1 means prerenal azotemia)
Plasma osmolality: 275 - 295 mOsm/kg H2O
Nephrotic syndrome
Glomeruli leaky to protein so get hypoalbuminemia
Frothy (protein-y) urine
Get edema all over (even in face) because decreased oncotic pressure and increased hydrostatic pressure in capillaries
Effective circulating volume decreases (b/c going into interstitum) and RAAS causes salt and water retention
