Renal Pathology

*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...

*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)

*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...

*During ACUTE rejection(usually before 6 months after transplant)Exposure to DONOR kidney antigens can induce BOTH humoral or Cellular immune response, thus morphology can be of 2 types:1)cellular response is mediated by CD8+Tcells that mediate Type IV hypersensitivity>Morpholical changes:Lymphocitic infiltrate of vessels>ENDOTHELIITIS,lymphocytic infiltrate of INTERSTITIUM>DIFFUSELY increased cellularity...2)HUMORAL response:antibodies develop AFTER transplantation(Contrast with preformed antibodies in hyperacute)>C4d deposits,NEUTROPHILC infiltrate,NECROTIZING VASCULITIS...vs*Calcineurin inhibitors(Which are often used to prevent acute rejection) can themselves damage kidney, specifically they DIRECTLY damage renal Endothelial and Tubular cells>Early arteriolar Hyalinization,TUBULAR Vacuolization.....<this actually showed up, i almost picked CD8 mediated damage but then i remembered that this was Expected Nephrotoxicity of drug....

*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)

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

*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....

*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)

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

*First of all FA calls it RBC cast but it is NOT, it is actually FATTY cast, which is associated with NephrOtic syndrome, these casts(oval fat bodies) when polarized produce characteristic Maltese cross(Due to presence of CHOLESTEROL which is always increased in neprhotic syndrome)

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

*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...

*Straddle fracture is basically result of bilateral fractures of superior and inferior pubic rami Most likely they will describe a case when patient rides a bike and has accident/Or false passage of transurethral cathether, then they will tell you that you see blood at urethral meatus and they can ask you about fascia involved(DEEP Fascia of Buck tear is the answer), but more likely they will ask about sites where urine can escape and answer to that is SUPERFICIAL PERINEAL SPACE, so remember damage of Anterior urethra(BULBAR/PENILE urethra) can result in leakage of urine into SUPERFICIAL PERINEAL SPACE(Space between Colles fascia and Inferior fascia of urogenital diaphragm) this space is continuous with SCROTAL sac,Space around penis,space on INFERIOR abdominal wall between abdominal muscles and Membranous layer of superficial fascia.....check the image and all will make sense(BTW it is not legal you have to draw it)

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

*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....