Nephrology Flashcards
Goodpasture disease
Autoimmune type 2 sensitivity reaction.
Lung symptoms usually precede kidney symptoms and include hemoptysis, cough, shortness of breath, and chest pain.
Kidney symptoms usually include blood and protein in the urine, unexplained edema, elevated blood pressures.
kidney biopsy: crescentic glomerulonephritis pathology with linear anti-GBM antibodies.
The 2 most important cause of metabolic acidosis with normal anion gap?
Renal tubular acidosis and diarrhea.
Renal tubular acidosis type I
The distal tubule cannot generate bicarbonate, the acid cannot be excreted into the tubule = raising the PH in the urine.
Renal tubular acidosis Type II
proximal tubule cannot reabsorb bicarbonate.
Renal tubular acidosis type IV
Occurs most often in diabetes
Decrease amount of effect of aldosterone=loss of sodium and retention of potassium and hydrogen ions.
Urine PH low
Patient shows signs of nephrotic syndrome and has Hodgkin’s lymphoma (HL), the nephropathy the patient is most likely experiencing?
The most common nephropathy associated with Hodgkin lymphoma and other hematologic malignancies minimal change disease.
The most common nephropathy associated with solid tumors is?
Membranous nephropathy (immune complex mediated).
Membranoproliferative glomerulonephritis
Nephrotic syndrome
Type I is generally a slower disease secondary to systemic lupus erythematosus (SLE), chronic hepatitis C, or hepatitis B. Type II is a more aggressive disease caused by autoimmune activation of complement by nephritic factor, an autoantibody against C3.
Both: low serum C3; however only type II is associated with C3 nephritic factor.
Biopsy: Type I, and type II shows intramembranous dense deposits.
Minimal change disease in adults
in association with Hodgkin’s and non-Hodgkin’s lymphomas and leukemia.
Most common cause of nephrotic syndrome in adults?
Focal segmental glomerulosclerosis
Hyposthenuria in sickle cell disease patients.
the defect in urinary concentration is related to sickled erythrocytes that restrict blood flow in the renal medulla, impairing the kidney’s ability to create a gradient needed to concentrate the urine.
Both antidiuretic hormone generation and urinary diluting capacity remain unperturbed.
Neither water deprivation nor desmopressin will result in a significant increase in urine osmolality.
The treatment of an acute exacerbation of Goodpasture syndrome?
Methylprednisolone, plasmapheresis, and cyclophosphamide.
Which other abnormality is autosomal dominant polycystic kidney disease associated with?
Polycystic liver disease, berry aneurysms and mitral valve prolapse (a mid-systolic click).
Metabolic alkalosis
Generated by four factors: volume depletion, chloride depletion, hypokalemia, and aldosterone excess.
These factors either increase the rate of bicarbonate reabsorption or decrease the rate of bicarbonate secretion.
Main clinical settings to consider:
- Loss of gastric fluid - nasogastric drainage or vomiting
- Diuretic therapy
- Mechanical ventilation of patients with chronic respiratory acidosis
- Primary hyperaldosteronism
Cooling dialysate benefits
Can improve hemodynamic stability, reduce hypotension, and improve cardiac function during hemodialysis. It may also reduce the risk of cardiovascular mortality and brain injury.
Acute kidney injury summary
Pre renal AKI oliguria, urine sodium <20meq/L, bun:cREAT >20:1, increase urine osmolarity, a low FENa (<1%).
Intrarenal AKI urine sodium <20meq/L, bun:CREAT <15:1, low urine osmolarity, a low FENa (>1%).
are unable to concetrate urine, a sign of a nephron damage.
Post renal AKI bun:cREAT <20:1, a low FENa (>1%), variable urine osmolarity, variable urine Na, depending on if it is early or late.
A diabetic patient with a non-anion gap metabolic acidosis, hyperkalemia, and renal insufficiency should be suspected of having?
Type 4 renal tubular acidosis
The lack of effect of aldosterone leads to decreased secretion of acid as ammonium (NH4+) and potassium retention.
Type 4 RTA may occur in the setting of diabetic nephropathy and can be exacerbated by drugs that inhibit the renin-angiotensin-aldosterone system, such as ACE inhibitors or ARBs.
Membranoproliferative glomerulonephritis
Nephrotic syndrome with two distinct forms.
Type I: Slower disease secondary to systemic lupus erythematosus, chronic hepatitis C, or hepatitis B.
Type II is a more aggressive disease caused by autoimmune activation of complement by nephritic factor, an autoantibody against C3.
Both share the laboratory findings of low serum C3.
Biopsy: Type I shown “tram-tracking” , and type II shows intramembranous dense deposits.
Treatment: prednisone with or without plasmapheresis or interferion-alpha, and prognosis is poor.
Renal osteodystrophy would present with?
Low calcium, high phosphate, and low energy fractures.
