Renal Pathology

1. A female develops middle-aged PALPABLE Purpura along with sudden onset of oliguria with proteinuria/RBC casts after a course of penicillin. She soon dies due to renal failure. A photograph shows glomeruli with proliferation of parietal epithelial cells in Bowman's capsule forming a crescent around the glomerulus. What antibodies are likely present in the patient's serum? (SUPER HY: Composition of crescents?)

*Patient has classic case of MICROSCOPIC Polyangitis precipitated by drug(Like penicillin),patient developed type 3 rapidly progressiveCRESCENTRIC glomerulonephritis>nEphritic presentation with RBC casts,proliferation of parietal epithelial cells in Bowman’s capsule forming a crescent around the glomerulus is classic finding for this PAUCI-immune glomeruloneprhitis(No Ig/C3), Patients with MICROSCOPIC POLYANGITIS often are positive for MPO-ANCA/P-ANCA....*Palpable purpura is More suggestive of microscopic polyangitis than Wegener granulomatosis(Which could also cause Pauci-immune glomerulonephritis, these patients would be positive for PR3-ANCA/C-ANCA) i just remember one to not confuse them, i remember later one by:I had to do CPR 3 times to bring Wegener alive)...*Well Crescents are composed of Fibrin,Macrophages,glomerular PARIETAL cells,Monocytes,plasma proteins(C3B), but most important(Testable) content is FIBRIN+MACROPHAGES so know them...

Anti-dsDNA antibodies

Anti-GBM antibodies

Antinuclear antibodies

The correct answer, MPO-ANCA/P-ANCA, is associated with MICROSCOPIC Polyangitis, which is a type of pauci-immune glomerulonephritis. Anti-GBM antibodies are found in Goodpasture's Syndrome. Anti-dsDNA antibodies are seen in systemic lupus erythematosus. Antinuclear antibodies are commonly found in autoimmune diseases like systemic lupus erythematosus and Sjogren's syndrome.

Explanation

The correct answer, MPO-ANCA/P-ANCA, is associated with MICROSCOPIC Polyangitis, which is a type of pauci-immune glomerulonephritis. Anti-GBM antibodies are found in Goodpasture's Syndrome. Anti-dsDNA antibodies are seen in systemic lupus erythematosus. Antinuclear antibodies are commonly found in autoimmune diseases like systemic lupus erythematosus and Sjogren's syndrome.

2. After upper airway infection, a young boy develops palpable purpura on buttocks, abdominal pain, and arthralgias. What are the most likely biopsy findings in this case? What are the C3 levels in serum?

The biopsy findings would reveal fibrinoid necrosis of blood vessel walls. The C3 levels in serum would be low.

*Palpable purpura in young boy, especially after recent URI is a giveaway for HSP-Kidney biopsy in this disease is characterized by MESANGIAL HYPERcellularity(proliferation) with igA and C3 staining of Mesangium(SUPER HY), also note that C3 levels in serum are NORMAL...they've asked about most likely progression of disease and that is Recovery(SELF-LIMITING) with high-rate of recurrence....BERGER disease(igA nephropathy) is basically KIDNEY pathology of HSP, IF shows igA based immune complexes in MESANGIUM...*HSP, Berger disease are common after URI,Enteritis because mucosal surfaces increase igA secretion in this conditions, don't confuse berger disease with bUErger disease(Segmental inflammation of MEDIUM-sized vessels associated with smoking,contrast this with HSP which is SMALL vessel vasculitis)

The biopsy findings would indicate perivascular infiltration of eosinophils. The C3 levels in serum would be elevated.

The biopsy findings would show granulomatous inflammation with giant cells. The C3 levels in serum would be elevated.

3. What is the most common Extraintestinal manifestation of ADPKD?

Hypertension

Pulmonary AVMs

Subarachnoid hemorrhage from rupture of Berry aneurysm

*COLONIC Diverticuli, however on boards they love to test the fact that these patients have hypertension and are at risk of SUBarachnoid hemorrhage due to RUPTURE of Berry aneurysm...

While patients with ADPKD are at risk of hypertension and subarachnoid hemorrhage from rupture of Berry aneurysm, the most common Extraintestinal manifestation is the presence of colonic diverticuli.

Explanation

While patients with ADPKD are at risk of hypertension and subarachnoid hemorrhage from rupture of Berry aneurysm, the most common Extraintestinal manifestation is the presence of colonic diverticuli.

4. Best ways to prevent urinary tract infections in patients with indwelling urinary catheters?

Frequent replacement of catheter

*FIRST-AVOID unnecessary chatheterization...use sterile technique when you insert it..*REMOVE catheter as fast as possible(NOT routine replacement of catheter-MC wrong answer,you only replace catheter if it is MUST, like with obstruction,infection)

Ignoring symptoms of urinary tract infection

Using non-sterile technique during catheter insertion

The best ways to prevent urinary tract infections in patients with indwelling urinary catheters include avoiding unnecessary catheterization, using sterile technique during insertion, and removing the catheter as soon as possible. Frequent replacement of catheters, using non-sterile technique, or ignoring symptoms of infection can actually increase the risk of urinary tract infections.

Explanation

The best ways to prevent urinary tract infections in patients with indwelling urinary catheters include avoiding unnecessary catheterization, using sterile technique during insertion, and removing the catheter as soon as possible. Frequent replacement of catheters, using non-sterile technique, or ignoring symptoms of infection can actually increase the risk of urinary tract infections.

5. Staghorn calculi(Like during Cystinuria)can be caused by defect in absorption of which type of amino acids?

Glycine

Aspartate

Glutamine

*Cystine, note that cystinuria is caused by defect in absorption of Positively charged basic amino acids(COLA-Cysteine,Ornithine,Lysine,Arginine)

Cystinuria is caused by a defect in the absorption of positively charged basic amino acids, specifically Cystine, Ornithine, Lysine, and Arginine (COLA).

Explanation

Cystinuria is caused by a defect in the absorption of positively charged basic amino acids, specifically Cystine, Ornithine, Lysine, and Arginine (COLA).

6. Site of pathology if WBC are present in urine vs WBC casts in urine?

Presence of WBC in urine indicates kidney pathology, while WBC casts suggest lower urinary tract involvement.

WBC in urine and WBC casts are interchangeable and do not provide information on site of pathology.

*Presence of WBC in urine likely indicated that patient has LOWER urinary tract pathology(Like Acute cystitis), WBC casts would be suggestive of involvement of KIDNEY(Glomerulus,Tubules) like in ACUTE PYELONEPHRITIS,Tubulointerstitial inflammation,transplant rejection....

Both WBC in urine and WBC casts indicate kidney involvement.

WBC in urine and WBC casts can help differentiate between lower urinary tract issues and kidney problems, providing important clues for diagnosis and treatment.

Explanation

WBC in urine and WBC casts can help differentiate between lower urinary tract issues and kidney problems, providing important clues for diagnosis and treatment.

7. What is the difference between RBC CASTS and RBCs present in urine?

RBC casts are indicative of a urinary tract infection, while RBCs present in urine indicate a kidney stone.

*RBC casts are suggestive of RENAL process,usually GLOMERULONEPHRITIS,Malignant hypertension vs just RBCs present in urine are suggestive of EXTRArenal process(Like bladder cancer)

RBC casts are specific to diabetic nephropathy, while RBCs present in urine indicate a kidney infection.

RBC casts are associated with polycystic kidney disease, while RBCs present in urine are a sign of dehydration.

8. What are casts often a manifestation of?

Diabetes mellitus

Acute kidney injury

Hypertension

*CHRONIC renal failure/ESRD(End-stage renal disease)...

Casts are often found in the urine of individuals with chronic renal failure or end-stage renal disease as a result of kidney damage and impaired filtration functions.

Explanation

Casts are often found in the urine of individuals with chronic renal failure or end-stage renal disease as a result of kidney damage and impaired filtration functions.

9. Granular (muddy brown) casts are associated with which condition?

Urinary tract infection

*ACUTE tubular necrosis....this can be a deadly condition and is often caused by drugs(like NSAIDs), so it is often tested on step1.

Glomerulonephritis

Chronic kidney disease

Granular (muddy brown) casts are associated specifically with acute tubular necrosis, which is often caused by drugs such as NSAIDs. It is crucial to differentiate this condition from others like chronic kidney disease, urinary tract infection, and glomerulonephritis.

Explanation

Granular (muddy brown) casts are associated specifically with acute tubular necrosis, which is often caused by drugs such as NSAIDs. It is crucial to differentiate this condition from others like chronic kidney disease, urinary tract infection, and glomerulonephritis.

10. What are the associations of Hyaline casts?

Parasitic infection, Glucosuria

*Viral infection,Proteinuria but can be seen just in concentrated urine samples and if they do test it will be likely integration with bIostat, the fact that it has LOW specificity and can be a normal finding...

Bacterial infection, Hematuria

Fungal infection, Leukocytosis

Hyaline casts are typically associated with viral infection, proteinuria, and can be seen in concentrated urine samples. It is important to note their low specificity and the possibility of being a normal finding in some cases.

Explanation

Hyaline casts are typically associated with viral infection, proteinuria, and can be seen in concentrated urine samples. It is important to note their low specificity and the possibility of being a normal finding in some cases.

11. Pelvic girdle fracture resulting in damage of MEMBRANOUS part of urethra (POSTERIOR urethra) could lead to escape of urine/blood into what space?

*RETROPUBIC space..escape can involve DEEP Perineal space and superiorly subperitoneal spaces around prostate and bladder.

Ischioanal space

Perirenal space

Pelvic cavity

In the case of damage to the membranous part of the urethra, urine or blood can escape into the retropubic space, involving deep perineal space and subperitoneal spaces around the prostate and bladder.

Explanation

In the case of damage to the membranous part of the urethra, urine or blood can escape into the retropubic space, involving deep perineal space and subperitoneal spaces around the prostate and bladder.

12. Which nerve is primarily responsible for erection?

SPINAL nerve (Somatic system)

*Erection is primarily mediated by PELVIC nerve(PARAsympathetic system)....under influence of Parasympathetic nervous system promotes release of NO from pelvic nerve> INCREASED cGMP(NOT cAMP)>Activate protein kinase G>dephosphorylation of MLCK>Relaxation of Smooth muscle>Vasodilation>Erection....

CRANIAL nerve (Autonomic system)

SURFACE nerve (Sympathetic system)

13. Nerve responsible for EJACULATION?

VAGUS nerve

FEMORAL nerve

SCIATIC nerve

*PUDENDAL nerve(SOMATIC nerve) which promotes RHYTHMIC contraction of bulbospongiosus muscle via SPINAL REFLEX....Ejaculation also has SYMPATHETIC(Visceral) component...

The correct nerve responsible for ejaculation is the PUDENDAL nerve, which is a SOMATIC nerve that promotes the rhythmic contraction of the bulbospongiosus muscle via SPINAL REFLEX. Ejaculation also involves a SYMPATHETIC (Visceral) component.

Explanation

The correct nerve responsible for ejaculation is the PUDENDAL nerve, which is a SOMATIC nerve that promotes the rhythmic contraction of the bulbospongiosus muscle via SPINAL REFLEX. Ejaculation also involves a SYMPATHETIC (Visceral) component.

14. Which nerve regulates the process by which sperm moves from testes to prostatic urethra?

Sciatic nerve

Femoral nerve

*Process described is EMISSION which is under control of sympathetic response of HYPOGASTRIC nerve...don't confuse this with ejaculation when sperm moves from prostatic urethra to outside...

Vagus nerve

The correct answer is the Hypogastric nerve, which controls the process of emission where sperm moves from the testes to the prostatic urethra under sympathetic response. The other three options are incorrect as they do not regulate this specific process.

Explanation

The correct answer is the Hypogastric nerve, which controls the process of emission where sperm moves from the testes to the prostatic urethra under sympathetic response. The other three options are incorrect as they do not regulate this specific process.

15. What are the effects of elevated levels of testosterone, LH, FSH, and inhibin in cryptoorchidism?

*Well here we test basic principles, you should know that NON-germ cells known as SERTOLI(SUSTENTICULAR)cells are TEMPERATURE sensitive, that means that these cells which line SEMINIFEROUS tubules can't produce [proper amounts of sperm and Inhibin B under conditions of higher temperatures(like during Cryptoorchidism when testes are in abdomen, or during varicocele)which they would normally produce, as they can't produce Inhibin B, FSH secretion will increase(normally is decreased by Inhibin B), BUT LH and testosterone levels will NOT be affected as Testosterone production happens in INTERSTITIAL cells of LEYDING(Endocrine cells) under influence of LH and levels of testosterone provide negative feedback on LH, as leyding cells are NOT affected by Temperature production of LH,Testosterone will Not be affected...So to sum up:LH,Testosterone levels will be normal, InhibinB concentration will be low, FSH concentration will be High, Sperm production will be low....for now at least know which cells line what and produce what

LH levels will be high, Testosterone levels will be low, FSH concentration will be high, Sperm production will be high

LH levels will be low, Testosterone levels will be high, FSH concentration will be low, Sperm production will be normal

LH and Testosterone levels will be high, Inhibin B concentration will be high, FSH concentration will be low, Sperm production will be normal

16. What is the endocrine function of sustenticular (Sertoli) cells?

Secreation of oxytocin, vasopressin, and growth hormone

Synthesis of LH, FSH, and prolactin

*seceretion of Inhibin B(inhibts FSH), Anti-mullerian hormone,ANDROGEN-binding protein(Sequesters Free testosterone keeps it at high concentration in Seminiferous tubules)....

Production of estrogen, progesterone, and testosterone

Sertoli cells are responsible for supporting and nourishing developing sperm cells in the seminiferous tubules of the testes. In addition to providing physical support, they also have important endocrine functions related to male hormone regulation and sperm development.

Explanation

Sertoli cells are responsible for supporting and nourishing developing sperm cells in the seminiferous tubules of the testes. In addition to providing physical support, they also have important endocrine functions related to male hormone regulation and sperm development.

17. Most important function of Sertoli cells?

*TIGHT junctions between them creates BLOOD-TESTES barrier which protects gametes from autoimmune barrier,sertoli cells also support/nourish developing spermatozoa...

They produce and release testosterone.

They are involved in the production of estrogen.

They regulate the release of FSH and LH hormones.

Sertoli cells primarily function to create a barrier between the blood and the testes to protect gametes and support the development of spermatozoa.

Explanation

Sertoli cells primarily function to create a barrier between the blood and the testes to protect gametes and support the development of spermatozoa.

18. Which cells line seminiferous tubules and maintain germ cell pool?

*SPERMATOGONIA(GERM CELLS) which produce PRIMARY spermatocytes, don't confuse this with Sertoli cells(Also line seminiferous tubules) but they Support developing spermatozoa and protect them from autoimmune attack..

Leydig cells

Interstitial cells

Sertoli cells

Sertoli cells support developing spermatozoa, Leydig cells produce testosterone, and Interstitial cells are found in the connective tissue surrounding seminiferous tubules.

Explanation

Sertoli cells support developing spermatozoa, Leydig cells produce testosterone, and Interstitial cells are found in the connective tissue surrounding seminiferous tubules.

19. What is the first step in treatment for a patient with PRIMARY FOCAL SEGMENTAL glomerulosclerosis?

*Blood Pressure control/ACE INHIBITORS/ARBs are best choice initially for FSGS because primary disease has inconsistent response to steroids....*Risk factors for SECONDARY FSGS are HY, they love Heroin use/HIV and Sickle cell disease but you should know that this condition is most common cause of nephrOtic syndrome in HISPANICS and AFRICAN-AMERICANS. you should also know that OBESITY, INTERFERON treatment can increase risk for FSGS too, now they tested association of congenital kidney malformation(MEDULLARY CYSTIC KIDNEY disease) with FSGS...MOST importantly EM findings of FSGS are very similar to findings characteristic for Minimal change disease(Affects children mainly), in both cases we often see effacement/FUSION of foot processes/focal damage of VISCERAL epithelial cells...note that minimal change disease is most common cause of nephrotic disease in children vs MCC of neprhotic syndrome in adults is FSGS(Not in Caucasian adults however where MCC is membranous nephropathy)...prognosis in FSGS is POOR,commonly progresses to CHRONIC renal failure(testable)

Begin immunosuppressive therapy to target the immune system

Consider surgical intervention to remove affected glomeruli

Administer high-dose steroids immediately

The correct initial treatment for FSGS is focused on blood pressure control and the use of ACE inhibitors/ARBs. Steroids may not be effective in the primary form of the disease, and surgical intervention is not typically recommended.

Explanation

The correct initial treatment for FSGS is focused on blood pressure control and the use of ACE inhibitors/ARBs. Steroids may not be effective in the primary form of the disease, and surgical intervention is not typically recommended.

20. In a Caucasian female with melanoma who develops proteinuria characteristic for Nephrotic syndrome, thickening of the glomerular basement membrane and capillary walls is seen on light microscopy. What are the expected findings on electron microscopy and what autoantibodies are involved in primary disease? Additionally, is this condition more strongly associated with HBV or HCV infection?

*GLOMERULAR BASEMENT MEMBRANE thickening along with nephrOtic syndrome in Caucasian adult with MELANOMA(or other cancers like colon carcinoma/Solid tumors in general), should make you think of MEMBRANOUS nephropathy(Membranous glomerulonephritis)which is MCC of Neprhotic syndrome in CAUCASIAN adults(Overall it is SECOND MCC cause of nephrotic syndrome in ADULTS after FSGS)*AUTOANTIBODIES involved in primary Membranous glomerulonephritis is super HY and autoantibodies against the podocyte protein M-type phospholipase A2 receptor (PLA2R) are implicated in this condition(High levels>poor prognosis), generally this condition doesn't respond well to steroids...*Electron microscopy findings include "Spike and Dome" appearance with SUBEPIthelial deposits(Don't confuse this with Subepithelial immune complex HUMPS of PSGN)....they LOVE to test IF findings of Membranous nephropathy and that is GRANULAR pattern(Due to Immune complex deposition contrast this with linear pattern where antibodies directly attach to Antigens in glomerular basement membrane)*Membranous nephropathy is more strongly associated with HBV while HCV is more strongly associated with membranoPROLIFERATIVE glomerulonephritis....they love to test association of membranous neprhopathy with PENICILLAMINE, but know that gold,NSAID use can precipitate it too and of course highly testable association with SLE and Solid tumors....*Malaria and syphilis have also been associated with this disease.note that Membranous nephropathy associated with SLE is RADICALLY different from LUPUS NEPHRITIS which is nephrItic syndrome associated with HIGH blood pressure,fever,HEMATURIA....

Expected findings on electron microscopy include 'Wire loop' lesions with mesangial proliferation. The primary autoantibodies involved in Membranous glomerulonephropathy are against the podocyte protein Nephrin. This condition is more strongly associated with HCV infection.

Expected findings on electron microscopy include 'Hump-shaped' subepithelial deposits. The primary autoantibodies involved in Membranous glomerulonephropathy are against the podocyte protein Podocin. This condition is more strongly associated with EBV infection.

Expected findings on electron microscopy include 'Crescent-shaped' glomerular tufts. The primary autoantibodies involved in Membranous glomerulonephropathy are against the tubular protein Aquaporin. This condition is more strongly associated with HIV infection.

21. What is the classic light microscopic finding for LIPOID NEPHROSIS (Minimal change disease)?

Cysts in glomeruli

Calcification of glomeruli

Hyaline deposits in glomeruli

*NORMAL GLOMERULI is seen on light microscopy, that's why it is called MINIMAL change disease, IF also doesn't usually yield abnormal findings HOWEVER EFFACEMENT of FOOT processes>Disruption of Glomerular filtration barrier/you loose filtration slits(grooves between them) and ALBUMIN is lost in the urine>PROTEINURIA with EDEMA, minimal change disease is MCC of NephrOtic syndrome in CHILDREN....*PRIMARY Idiopathic disease usually follows some type of immune stimuli like after immunizaiton(Yet it is still idiopathic cause the exact reason is unknown) and has EXCELLENT Respnose to Corticosteroids, HOWEVER if child presents with nephrotic syndrome you should also suspect possible LYMPHOMA as Secondary MInimal change disease can be due to CYTOKINE-MEDIATED damage associated with Lymphoma...

Minimal change disease is characterized by the presence of normal glomeruli on light microscopy, which is why it is called 'minimal change disease'.

Explanation

Minimal change disease is characterized by the presence of normal glomeruli on light microscopy, which is why it is called 'minimal change disease'.

22. Why do patients with nephrotic syndrome have a higher risk of hypercoagulable states?

Loss of von Willebrand factor in the bloodstream

*Due to Loss of ANTIthrombin III in the urine....

Increased production of antithrombin III

Decreased platelet aggregation

Patients with nephrotic syndrome often have increased urinary loss of antithrombin III, which is an important inhibitor of blood clot formation. This imbalance can result in a hypercoagulable state, increasing the risk of blood clots.

Explanation

Patients with nephrotic syndrome often have increased urinary loss of antithrombin III, which is an important inhibitor of blood clot formation. This imbalance can result in a hypercoagulable state, increasing the risk of blood clots.

23. Why are patients with Neprhotic syndrome at increased risk of infection?

Because patients with Neprhotic syndrome have decreased permeability of blood vessels, making them more susceptible to invading pathogens

*Because immunoglobulins are needed to fight off infections, immunoglobulins are proteins and proteins are lost in large quantities during nephrOtic syndrome+They have edema(Due to loss of oncotic pressure),edema can promote formation of Skin ulcer(Compression of small blood vessels>Dead tissue>Pressure ulcer) and DELAY Wound healing....

Because their immune system is overactive, leading to a higher susceptibility to infections

Because Neprhotic syndrome causes an increase in white blood cell count, making it easier for infections to take hold

24. What mechanism leads to MESANGIAL expansion in Diabetic glomerulonephropathy?

*MESANGIAL expansion is characteristic for Diabetic glomerulonephropathy and is due to HYPERFILTRATION damage(HYALINE arteriolosclerosis of Efferent arteriole>INCREASED GFR which eventually can lead to Mesangial expansion),that's why ACE inhibitors/ARBs are great to treat Diabetic neprhopathy/Hypertenison in those patients as they decrease GFR by dilation of Efferent arteriole...*Now EOSINOPHILIC Nodular masses in mesangial matrix are known as Kimmelstiel-Wilson lesions which represent EXCESSIVE type IV collagen deposition along with protein trapping...GBM is thickened and is more permeable to proteins(Leading to nephrOtic syndrome) due to NONenzymatic GLYCOSYLATION of GBM that happen at persistent High glucose levels....ANSWER for question:test that can be used for SCREENING of EARLY diabetic neprhopathy? URINE MICROalbumin test(albumin begins to leak into the lumen as glomerulus starts to weaken)

Tubular atrophy

GLOMERULAR hypertrophy

Podocyte dysfunction

The MESANGIAL expansion in Diabetic glomerulonephropathy is primarily due to HYPERFILTRATION damage caused by HYALINE arteriolosclerosis of the Efferent arteriole, leading to increased GFR and subsequent Mesangial expansion.

Explanation

The MESANGIAL expansion in Diabetic glomerulonephropathy is primarily due to HYPERFILTRATION damage caused by HYALINE arteriolosclerosis of the Efferent arteriole, leading to increased GFR and subsequent Mesangial expansion.

25. What is the significance of Basket-weave appearance on EM?

Basket-weave appearance indicates presence of membranous nephropathy.

*Alport disease is SUPER HY and you should think of it when patient has signs of nephrItic syndrome+Occular problems(Like retinopathy) and/or SENSORINEURAL(NOT CONDUCTING) deafness(Highly testable)...*Basket-weave appearance is classic finding on electron microscopy that is basically a description for SPLIT basement membrane which shows irregular THINING+THICKENING creating LAMELLATED Basket-weave appearance.this defect in basement membrane is due to mutation in COL4A5 which codes for component of type IV collagen(SUPER HY)...this disease is special because it is X-linked DOMINANT(like Fragile X syndrome), they tend to test inheritanec of X-linked DOMINANT diseases in this way: they'll ask about chance of affected father who marries normal wife to have Girls affected by this disease and answer is 100%, remember Man gives 1 X to every girl, he has only 1 X as he is a male, this 1 X is affected with this DOMINANT allele so even though they receive another X with normal allele from mommy, DOMINANT allele from X of daddy>Affected, HOWEVER they tend to love another interesting fact with X-linked Dominant diseases, they might describe such a case and tell you that daughter is NOT affected by the disease and ask you WHY and answer is RANDOM X inactivation (remember only X chromosome is expressed ,another one is silenced and turns into barr body, this process is completely random so manifestations of X-linked dominant disorders, or even for X-linked recessive disorders can vary due to this phenomenon) X-linked Dominant, it produces nephrItic syndrome and Sensorineural deafness and primarily involves defect in Type 4 collagen leading to splitting/irregular apperance of basement membrane....

Basket-weave appearance is a sign of IgA nephropathy.

Basket-weave appearance is seen in patients with minimal change disease.

The correct answer highlights the specific association of Basket-weave appearance with Alport disease, which is linked to a mutation in COL4A5 gene causing irregular thinning and thickening of the basement membrane. The incorrect answers provide common misconceptions about other renal conditions related to EM findings, illustrating the importance of recognizing the unique implications of Basket-weave appearance.

Explanation

The correct answer highlights the specific association of Basket-weave appearance with Alport disease, which is linked to a mutation in COL4A5 gene causing irregular thinning and thickening of the basement membrane. The incorrect answers provide common misconceptions about other renal conditions related to EM findings, illustrating the importance of recognizing the unique implications of Basket-weave appearance.

26. Patient with Mixed Neprhotic/Nephritic picture(like Proteinuria of >3.5 g/day suggestive of nephrotic syndrome yet fever, hypertension, RBC casts suggestive of nephritic syndrome), he has History of HCV...on Silver stain we see DOUBLE Contour of glomerular basement membrane ("Tram-Tracking)", what is the mechanism? What are the characteristic findings on IF? What is nephrItic factor?

*This is classic description of MPGN, mechanism of tram tracking is Splitting of basement membrane by ingrowth of mesangium...Type I MPGN is associated with HCV and HBV infections(But more with HCV) and is characterized by subendothelial(NOT subepithelial) immune complex deposits with granular IF....if they also mention C3 nephritic factor than you should pick DENSE CORE DISEASE as answer, Dense core disease=Type II MPGN, you have deposition of dense material of UNKNOWN origin, however type II MPGN is associated with nephrItic syndrome which is basically igG immunoglobulin that stabilizes C3 convertASE that leads to persistent COMPLEMENT activation>Depletion of C3>decreased serum C3 levels....

This is a description of minimal change disease (MCD), characterized by a normal glomerular basement membrane and idiopathic nephrotic syndrome with no systemic manifestations.

The scenario fits the criteria for IgA nephropathy, which is characterized by mesangial immune complex deposits and hematuria but not necessarily the double contour of the glomerular basement membrane or association with HCV.

The patient likely has focal segmental glomerulosclerosis (FSGS), which presents with nephrotic syndrome and hypertension but no history of HCV infection. Tram-tracking is not a common finding in FSGS.