Nephrology

Question 1

What is PIGN?

Answer 1

A glomerulonephritis that occurs following URTI characterized by low C3, proteinura, hematuria, hypertension, edema and elevated creatinine

Question 2

What is the management of PIGN?

Answer 2

Sodium and water restrict, Furosemide (loop diuretic), occasionally Nifedipine or calcium channel blocker

Question 3

What is the nutcracker syndrome?

Answer 3

Compression of left renal vein between the aorta and superior mesenteric artery causing hematuria and can cause flank/abdo pain

Question 4

What are the characteristics of nephritic syndrome?

Answer 4

Proteinuria
Hematuria
Azotemia (elevated Cr/urea)
RBC casts
Oliguria
HTN

Question 5

What are the characteristics of nephrotic syndrome?

Answer 5

Hypoalbuminemia (<25g/L)
Edema
Lipidemia
Proteinura (3g/L or 3+ on urine dipstick)

Question 6

What are the risks of nephrotic syndrome?

Answer 6

Infection by encapsulated organisms due to loss of immunoglobulins and complement, increased risk of thrombosis due to loss of anti-thrombin through urine

Question 7

What are the causes of nephrotic syndrome?

Answer 7

Minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, medications (NSAIDs, lithium, etc.), infections (HIV, Hepatitis B, Hepatitis C), malignancy (leukemia/lymphoma)

Question 8

Causes of heme-negative red urine

Answer 8

Doxorubicin, Nitrofurantoin, Rifampin, beets, methemoglobin, Porphyrin

Question 9

What is IgA nephropathy?

Answer 9

Gross, painless hematuria that tends to occur concomitant with infection. Due to IgA deposits in the kidney, some may present with microscopic hematuria +/- proteinuria only. C3 is normal and some patients may have elevated IgA levels

Question 10

What is the prognosis of IgA nephropathy?

Answer 10

The higher the prevalence of proteinuria, especially between episodes, the worse the prognosis. Risk of ESRD is 20%

Question 11

What is HSP (IgA vasculitis)?

Answer 11

A small vessel vasculitis causing deposits of IgA in multiple organs, particularly kidneys. It is characterized by non-thrombocytopenia palpable purpuric rash, nephritic syndrome, GI manifestations and arthralgia/arthritis. Nephritis tends to be the last manifestation presenting at 8 weeks after initial presentation

Question 12

What is hemolytic uremic syndrome?

Answer 12

Classic triad of microangiopathic hemolytic anemia, thrombocytopenia, renal dysfunction

Question 13

What is hemolytic uremic syndrome triggered by?

Answer 13

Classically by e.coli O157:H7 that produces shiga toxin. Presents as bloody diarrhea. Can also be triggered by Strep pneumo, HIV, HHV-6, etc. and strep pneumo triggered is DAT positive

Question 14

What are the indications for dialysis?

Answer 14

Acidosis
Electrolyte abnormalities
Intoxications
Oliguria/overload of fluids
Uremia

Question 15

What are insensible losses?

Answer 15

400mL/m2/day

Question 16

What is Alport syndrome?

Answer 16

Mutation in one of the genes (COL4) encoding one of the alpha chains of type 4 collagen. X-linked disorder. Leads to SNHL, microscopic hematuria and eventual proteinuria and renal disease, retinopathy/anterior lens capsule

Question 17

What are the abnormal ranges for proteinuria?

Answer 17

For 24 hour collection, >4mg/m2/day is abnormal
For protein:creatinine ratio >20mg/mmol is abnormal
For albumin:creatinine ratio >30mg/mmol is abnormal
C-P-A: 4 - 20 - 30

Question 18

What are the concerning organisms for spontaneous bacterial peritonitis in nephrotic syndrome?

Answer 18

Some Nasty Killers Have Serious Capsule Protection

Strep pneumo
Neisseria meningitides
Klebsiella pneumoniae
Haemophilus influenzae type B
Salmonella typhi
Cryptococcus neoformans (fungi)
Psuedomonas aeruginosa

Question 19

What is thin basement membrane nephropathy?

Answer 19

Also known as benign familial hematuria, defect in COL4A3 or COL4A4 causing microscopic hematuria that may be intermittent or persistent. Usually have no other signs of significant renal disease but in some families it can

Question 20

What are the criteria to make the diagnosis of SIADH?

Answer 20

Euvolemic hyponatremia with low serum osmolality, high urine osmolality, high urine sodium. Also have low plasma uric acid and low plasma BUN

Question 21

What do you see in psychogenic polydypsia?

Answer 21

Hyponatremia but low urine osmolality as your kidney’s are working appropriately and excreting the excess water as much as possible, they are just getting overwhelmed

Question 22

What is seen in cerebral salt wasting?

Answer 22

Urine output is high as water is following the salt you’re losing. Urine sodium and urine osmolality are both high. Serum sodium low and intravascularly deplete. Seen in ICU patients, brain bleeds

Question 23

What is anion gap formula? The osmolar gap?

Answer 23

AG = Na - (Cl +HCO3)
OG = 2(Na) - glucose - BUN

Question 24

What is the formula to calculate a urine anion gap?

Answer 24

Urine AG = (Na + K) - Cl

Question 25

What are the types of RTAs and features?

Answer 25

Type 2 (Proximal tubule) - low potassium, lose amino acids, glucose, phosphate, uric acid. Urine pH <5.5. Fanconi syndrome causes
Type 1 (Distal tubule) - low potassium, high urine pH as acidification is affected. Secrete calcium into urine and have low urine citrate, so get nephrocalcinosis. 
Type 4 (Collecting tubule) is a hypoaldosteronism- high potassium, urine pH <5.5

Question 26

What is cystinosis?

Answer 26

Autosomal recessive lysosomal storage disorder. Cystine accumulates in lysosome and most common cause of Fanconi syndrome in children (type 2 RTA, low phosphate, uric acid, glucose, poor growth, FTT)

Question 27

What is Bartter syndrome?

Answer 27

Looks like chronic furosemide use, genetic defect causes decreased activity in one of several electrolytes transporters in the thick ascending loop of Henele causing impaired NaCl absorption, polyuria and polydipsia, volume depletion, activation of RAAS, hypokalemia, metabolic alkalosis, high urine calcium