MEDICINE NEPHROLOGY FINAL
ASSESSMENT PREPARATION PAPER 2026
HIGH YIELD RENAL CONCEPTS AND
ANSWERS
◉ • Post-infectious cause of nephritic syndrome. Most commonly
occurs after a group-A-beta hemolytic streptococcus infection
including impetigo or strep throat 10-14 days prior. Whether it was
treated or not.
• Diagnosis through ASO titers, low serum complement-3 - not
usually done as this disease is usually self-limiting.
• Supportive. Antibiotics if needed.
Answer: • What is the post-infectious glomerulonephritis?
• Diagnosis?
• Treatment?
◉ Membranoproliferative Glomerulonephritis
Answer: Thick glomerular basement membrane due to immune-
complex deposition, which then cause nephritic syndrome. Due to
SLE, viral or hepatitis B or C, hypocomplementemia. Has a mixed
nephritic/nephrotic presentation.
,◉ Rapidly Progressive Glomerulonephritis
Answer: Nephritic syndrome that progresses to renal failure in
weeks to months. Usually this disease is considered to have a poor
prognosis. On biopsy, a crescent formation is seen which is due to
protein and sclerosing deposition within Bowman's capsule
collapsing it and rendering it non-functional.
◉ Vasculitis
Answer: Inflammation of blood vessels. Microscopic polyangiitis and
Wegener's are vasculitis diseases of small/medium-sized vessels
and are both ANCA-antibody positive. Vasculitis diseases attack
small vessels including the kidney.
◉ Goodpasture Disease
Answer: Disease that causes nephritic syndrome through anti-
glomerular basement membrane antibodies versus the type IV
collagen seen in both the kidneys and lungs. The resulting clinical
manifestations are kidney failure with hemoptysis as the anti-GBM
antibodies damage the basement membrane of the lungs and kidney.
Can occur after a URI in which antibodies are produced that
accidentally recognize this type IV collagen. Treatment: high-dose
corticosteroids PLUS cyclophosphamide. Sometimes plasmapheresis
is used to remove antibodies.
,◉ • Disease that causes nephritic syndrome through anti-glomerular
basement membrane antibodies versus the type IV collagen seen in
both the kidneys and lungs.
• The resulting clinical manifestations are kidney failure with
hemoptysis as the anti-GBM antibodies damage the basement
membrane of the lungs and kidney. Can occur after a URI in which
antibodies are produced that accidentally recognize this type IV
collagen.
• High-dose corticosteroids PLUS cyclophosphamide. Sometimes
plasmapheresis is used to remove antibodies.
Answer: • What is Goodpasture disease?
• Clinical presentation?
• Treatment?
◉ Nephritic vs Nephrotic Syndrome
Answer: *Nephrotic Syndrome*
• Significant proteinuria. Urine albumin > 3.0-3.5 q 24 hrs
• Serum albumin low (< 3.5)
• +/- hematuria
• Significant edema
• Normal blood pressure
• No RBC casts
• Hyperlipidemia and lipiduria. Urine protein Cr > 3 g
*Nephritic Syndrome*
, • Mild proteinuria
• Normal, very mild decrease in serum albumin
• Significant hematuria
• +/- edema
• Elevated blood pressure
• RBC casts present
• Decreased GFR, oliguria
◉ Renal Vascular Disease
Answer: Progressive condition that causes blockage of the renal
arteries or veins. The two major conditions that lead to this blockage
are: renal artery stenosis and renal artery fibromuscular dysplasia.
These conditions lead to decreased perfusion to the kidneys, which
tricks the kidneys into thinking that the blood pressure is much
lower than it really is. This leads to an increase in the RAAS which
increases BP by increasing sympathetic stimulation and sodium
reabsorption. HTN leads to end-organ damage, especially in
microvasculature including the eyes, kidneys, brain, and extremities.
Clinical presentation: abdominal bruit, HA, severe/refractory HTN.
Diagnosis through CT, US, or MR angiography. Renal arteriography is
gold standard. Treatment: ACE inhibitors or ARBS. However, if
bilateral renal artery stenosis or only one kidney. ACE inhibitors and
ARBs are contraindicated. This is because GFR and renal perfusion is
decreased in these patients, which can lead to AKI. Surgical:
angioplasty with stent.
ASSESSMENT PREPARATION PAPER 2026
HIGH YIELD RENAL CONCEPTS AND
ANSWERS
◉ • Post-infectious cause of nephritic syndrome. Most commonly
occurs after a group-A-beta hemolytic streptococcus infection
including impetigo or strep throat 10-14 days prior. Whether it was
treated or not.
• Diagnosis through ASO titers, low serum complement-3 - not
usually done as this disease is usually self-limiting.
• Supportive. Antibiotics if needed.
Answer: • What is the post-infectious glomerulonephritis?
• Diagnosis?
• Treatment?
◉ Membranoproliferative Glomerulonephritis
Answer: Thick glomerular basement membrane due to immune-
complex deposition, which then cause nephritic syndrome. Due to
SLE, viral or hepatitis B or C, hypocomplementemia. Has a mixed
nephritic/nephrotic presentation.
,◉ Rapidly Progressive Glomerulonephritis
Answer: Nephritic syndrome that progresses to renal failure in
weeks to months. Usually this disease is considered to have a poor
prognosis. On biopsy, a crescent formation is seen which is due to
protein and sclerosing deposition within Bowman's capsule
collapsing it and rendering it non-functional.
◉ Vasculitis
Answer: Inflammation of blood vessels. Microscopic polyangiitis and
Wegener's are vasculitis diseases of small/medium-sized vessels
and are both ANCA-antibody positive. Vasculitis diseases attack
small vessels including the kidney.
◉ Goodpasture Disease
Answer: Disease that causes nephritic syndrome through anti-
glomerular basement membrane antibodies versus the type IV
collagen seen in both the kidneys and lungs. The resulting clinical
manifestations are kidney failure with hemoptysis as the anti-GBM
antibodies damage the basement membrane of the lungs and kidney.
Can occur after a URI in which antibodies are produced that
accidentally recognize this type IV collagen. Treatment: high-dose
corticosteroids PLUS cyclophosphamide. Sometimes plasmapheresis
is used to remove antibodies.
,◉ • Disease that causes nephritic syndrome through anti-glomerular
basement membrane antibodies versus the type IV collagen seen in
both the kidneys and lungs.
• The resulting clinical manifestations are kidney failure with
hemoptysis as the anti-GBM antibodies damage the basement
membrane of the lungs and kidney. Can occur after a URI in which
antibodies are produced that accidentally recognize this type IV
collagen.
• High-dose corticosteroids PLUS cyclophosphamide. Sometimes
plasmapheresis is used to remove antibodies.
Answer: • What is Goodpasture disease?
• Clinical presentation?
• Treatment?
◉ Nephritic vs Nephrotic Syndrome
Answer: *Nephrotic Syndrome*
• Significant proteinuria. Urine albumin > 3.0-3.5 q 24 hrs
• Serum albumin low (< 3.5)
• +/- hematuria
• Significant edema
• Normal blood pressure
• No RBC casts
• Hyperlipidemia and lipiduria. Urine protein Cr > 3 g
*Nephritic Syndrome*
, • Mild proteinuria
• Normal, very mild decrease in serum albumin
• Significant hematuria
• +/- edema
• Elevated blood pressure
• RBC casts present
• Decreased GFR, oliguria
◉ Renal Vascular Disease
Answer: Progressive condition that causes blockage of the renal
arteries or veins. The two major conditions that lead to this blockage
are: renal artery stenosis and renal artery fibromuscular dysplasia.
These conditions lead to decreased perfusion to the kidneys, which
tricks the kidneys into thinking that the blood pressure is much
lower than it really is. This leads to an increase in the RAAS which
increases BP by increasing sympathetic stimulation and sodium
reabsorption. HTN leads to end-organ damage, especially in
microvasculature including the eyes, kidneys, brain, and extremities.
Clinical presentation: abdominal bruit, HA, severe/refractory HTN.
Diagnosis through CT, US, or MR angiography. Renal arteriography is
gold standard. Treatment: ACE inhibitors or ARBS. However, if
bilateral renal artery stenosis or only one kidney. ACE inhibitors and
ARBs are contraindicated. This is because GFR and renal perfusion is
decreased in these patients, which can lead to AKI. Surgical:
angioplasty with stent.
