First Aid: Renal Flashcards
A neonate presents with limb deformities, facial anomalies (low set ears and retroganthia), chest compression and pulmonary hypoplasia. What is this fetus suffering from and what are some possible causes?
POTTER Syndrome Pulmonary hypoplasia Oligohydramnios (trigger) Twisted face Twisted Skin Extremity Defects Renal Failure (in utero)
Causes: ARPKD, posterior urethral valves, bilateral renal agenesis
What are patients with Horseshoe kidney at increased risk of developing? What major syndrome is this condition associated with?
- Increased risk for ureteropelvic junction obstruction
- hydronephrosis
- renal stones
- rarely renal cancer (Wilms Tumor)
Associated with Turner syndrome
Abnormal interaction between ureteric bud and metanephric mesenchyme (which leads to glomerular development) results in what condition?
Multi cystic dysplastic kidney - nonfunctioning kidneys with cysts and connective tissue
Asymptomatic if unilateral, with compensatory Hypertrophy of opposite kidney
What is a main concern in a procedure like hysterectomy?
Ligation of uterine vessels may damage the ureter leading to ureteral obstruction or leak.
“Water under the bridge”
In which condition is the charge barrier lost for glomerular filtration? What results?
Nephrotic Syndrome
Albuminuria, hypoproteinemia, generalized edema, hyperlipidemia
Where do NSAIDs exert their effects on the glomerulus? What about ACE inhibitors?
Normally prostaglandins dilate afferent arterioles, so NSAID will block here and cause constriction.
Normally Angiotensin II constricts efferent arterioles, so ACE INHIBITORS will block here causing dilation.
A patient is administered an NSAID, what would happen to the filtration fraction? What about if ACE inhibitors were given?
FF = GFR / RPF
NSAID –> constriction of afferent arteriole (normally prostaglandins would dilate) –> decrease RPF and GFR –> FF remains constant
ACEI –> dilation of efferent arteriole (normally angiotensin II would constrict) –> increase RPF and decrease GFR –> FF decreases
Think the opposite without the presence of drug
A pregnant woman gives a urine sample. What would you expect of glucose and amino acid levels?
During pregnancy it is normal to have decreased reabsorption of glucose and amino acids at proximal tubule, so you would see glucosuria and aminoaciduria.
Plasma glucose of 200 mg/dL is threshold for glucosuria to begin, at 375 mg/dL all transporters in proximal tubule become saturated
A patient presents with neutral aminoaciduria and decreased absorption of these amino acids in the gut. They have pellagra like symptoms. What should you treat them with?
Hartnup Disease - autosomal recessive disorder - decreased reabsorption of neutral amino acids in renal tubular cells and enterocytes.
Treat with high protein diet and nicotinic acid
What two things will increase water reabsorption in the collecting tubules? What two things will decrease water reabsorption here?
Aldosterone increases Na channel insertion on lumen –> increased Na absorption –> increased H2O absorption
ADH Mobilized aquaporins, increasing H2O reabsorption
Potassium sparing diuretics will counteract and increase H2O excretion: the K+ STAys –> Spironolactone (aldosterone receptor antagonist), Triamtrene, Amiloride (blocks Na channels)
Name all of the renal tubular defects, the resultant dysfunction and if applicable, their causes.
“The kidneys put out FABulous Glittering Liquid.”
FAnconi syndrome (PCT): increased excretion of all amino acids, glucose, bicarb, and phosphate. Hereditary defects (Wilson Disease), ischemia, nephrotoxins/drugs.
Bartter Syndrome (thick ascending loop): AR affecting Na/K/2Cl cotransporter. Hypokalemia and metabolic alkalosis w/ hypercalcuria.
Gitelman Syndrome (DCT): AR, reabsorptive defect of NaCl. Hypokalemia and metabolic alkalosis, NO hypercalcuria.
Liddle Syndrome (collecting ducts): AD, increased Na reabsorption. HTN, hypokalemia, metabolic alkalosis, decreased aldosterone.
What factors will induce the kidneys to secrete renin? What is responsible for secreting renin?
- decreased BP (JG cells)
- decreased Na delivery (macula densa cells)
- increased sympathetic tone (beta-1 receptors)
- Tumors - paraneoplastic syndrome
Juxtaglomerular apparatus
What are the major affects of Angiotensin II on the body? What occurs on the organ level to allow for this?
Helps maintain blood volume and blood pressure, while limiting reflex bradycardia.
Increased reabsorption of Water and Salt, increased excretion of K+ and H+.
Overall vasoconstriction. Preferential constriction of efferent arteriole.
What compound acts as a “check” on the renin-angiotensin -aldosterone system? What results from its action?
Atrial Natriuretic Peptide (ANP) - which relaxes vascular smooth muscle via cGMP causing increased GFR and decreased renin.
There is also increased Na filtration without compensatory increased reabsorption. Net Na and volume loss.
From where is erythropoietin released?
Interstitial cells in the peritubular capillary beds (in response to hypoxia).
What induces the release of ADH? What about PTH?
What is the result of their action?
ADH - increased plasma osmolarity, decreased blood volume. Causes increased H2O reabsorption.
PTH - decreased Ca, increased Phsophate, decreased vitamin D. Causes increased Ca reabsorption (DCT), decreased phosphate reabsorption (PCT) and increased Vit D production
What are the possible factors for inducing hyperkalemia in patients?
DO Insulin LAB work. INsulin shifts K+ INto cells.
Digitalis hyper-Osmolarity INSULIN deficiency Lysis of cells Acidosis Beta-adrenergic antagonist
A patient presents with low pH and low pCO2. They are hyperventilating. What do you want to check next and how?
Metabolic acidosis with compensation –> Check ANION GAP
Anion Gap = Na+ - (Cl- + HCO3-)
A patient presents with flank tenderness, hematuria, colicky pain radiating to groin, and abdominal pain. They seem to be very anxious and are confused. What ion may there be a high serum concentration of?
Calcium
Stones (renal), bones (pain), groans (abdominal pain), psychiatric overtones (anxiety, altered mental status).
Will not necessarily have calciuria.
A hyperventilating patient with metabolic acidosis has a high anion gap (»12 mEq/L). What are the possibilities for this condition? What if the anion gap was normal (8-12 mEq/L)?
High anion gap = MUDPILES Methanol (formic acid) Uremia Diabetic Ketoacidosis Propylene glycol Iron tablets or INH Lactic Acidosis Ethylene glycol (oxalic acid) Salicylates (late)
Normal anion gap = HARD ASS Hyperalimentation Addison Disease Renal tubular acidosis Diarrhea Acetazolamide Spironolactone Saline infusion
A patient presents with massive proteinuria (>3.5g/day, frothy urine), hyperlipidemia, edema, and fatty casts in the urine. What other problems may this person’s disorder be associated with and why?
NephrOtic Syndrome
Hypoalbuminemia and Hyperlipidemia already mentioned also can have,
- Hypercoaguable state - Thromboembolism (due to ATIII loss in urine)
- Hypogammaglobulinemia - increased risk of infection (loss of immunoglobulins)
A young AA woman who is HIV+ presents with massive proteinuria, edema and fatty casts in urine. They have a fever and show signs of infection. A kidney biopsy is taken. What would you see on histology, IF and EM? What are the other associations for this person’s disorder?
Focal Segmental Glomerulosclerosis (NOS) - inconsistent response to steroid therapy
Histo: Segmental sclerosis of a glomerulus and hyalinosis (pink staining)
IF negative
EM: Effacement of foot process
Most common NOS in AAs and Hispanics. Associated with HIV infection, sickle cell, heroin abuse, massive obesity, interferon treatment, and chronic kidney disease due to congenital absence or surgical removal.
A middle aged white man presents with massive proteinuria, fatty casts in urine and edema. He was otherwise in normal health, had no major disease or infections in the past, and was not taking any drugs. A kidney biopsy is taken and reveals diffuse capillary and glomerular basement membrane thickening on light microscopy. What would IF and EM reveal? What are the common associations for his condition?
Membranous Nephropathy - poor response to steroid therapy
IF - positive, granular, from immune complex deposition
EM - “spike and dome” appearance with subepithelial deposits of the immune complexes
Associated with antibody phospholipase A2 receptor, drugs (NSAIDs & penicillamine), infections (HBV, HCV), Lupus, solid tumors.
A young girl presents with symptoms consistent with Nephrotic Syndrome. Her mother states that she recently had a bad case of the cold. A biopsy reveals normal glomeruli on light microscopy with some lipid in the PCT cells. What would you see on IF and EM? What would be the next step in care?
Minimal Change disease (lipoid nephrosis) - Triggered by recent infection, immunization or immune stimulus. May be associated with Hodgkin lymphoma.
IF - Negative
EM - Effacement of foot processes
Give CORTICOSTEROIDS - Excellent response
In minimal change disease all kinds of protein can be lost in the urine, True or False?
False
Selective proteinuria (loss of albumin but NOT immunoglobulin)
A patient has systemic amyloidosis, what is the most likely affected organ? What would biopsy reveal?
Kidney is most commonly involved. Associated with chronic conditions (e.g. multiple myeloma, TB, rheumatoid arthritis).
LM - congo red stain shows apple-green birefringence under polarized light
Compare and contrast the key differences between Type 1 and Type 2 Membrano-proliferative glomerulonephritis:
Type 1: Subendothelial IM complex deposits w/ mesangial ingrowth that gives “TRAM TRACK” apperance. Granular + IF. Associated w/ HBV/HCV or idiopathic.
Type 2: Intramembranous IC “DENSE” deposits. Associated w/ C3 nephritic factor auto-antibody.
Describe the immune process that results in Type 2 MPGN:
C3 nephritic factor auto antibody stabilizes C3 convertase, increasing formation of complement, leading to infection and subsequent glomerular damage
