Kidney Pathology

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Kidney Pathology by Mind Map: Kidney Pathology

1. Hydronephrosis

1.1. Causes

1.1.1. Obstruction

1.1.2. Compression

1.2. Who

1.2.1. fetus cause unknown often resolves

1.2.2. Third Trimester vesicouretal reflex retrograde flow of urine from bladder into urinary tract congenital uretopelvic obstruction problem/blockage of urine leaving renal pelvis

1.2.3. young child Congentital malformations uretoerocele posterior urethral valves

1.2.4. Adults Acquired Disease Kidney Stones BPH

1.3. Presents with

1.3.1. Obstructive Flank Pain Groin Pain UTI

1.3.2. Hydronephrosis post renal azotemia increased N reabsoprtion

1.4. DX:

1.4.1. US

1.4.2. Intrauretal urography

1.4.3. Intrauretal pyelography

1.4.4. CT

1.5. Tx:

1.5.1. relieve obstruction acute nephrostomy tube Chronic Ureteric stent Pyeloplasty Lower obstruction Urinary catheter Suprapubic catheter

2. Congenital

2.1. Horshoe Kidney

2.1.1. How 1- Mechanical Fusion at 5 wks (metanephros) flexion pushes kidneys together inferior poles touch and fuse leads to isthmus 2-Teratogenic event Posterior Nephrogenic cells migrate to posterior pole of kidney (wrong spot) leads to isthmus

2.1.2. Complications Stuck on Inferior mesenteric artery on ascention leads to lower placement can cause compression of kidney can cause hydropnephrosis

2.1.3. associations Kidney stones Infection Chromosomal Disorders Turner Trisomies 13,18,21 increased risk of kidney cancer

2.1.4. Demographics common 1:500 men>women

2.1.5. Symptoms normally asymptomatic

2.1.6. Tx normally not necessary might need sx if leads to complication

2.2. Obstructive (see Hydronephrosis)

2.2.1. Primary Vesicouretal Reflux Notes Most common Pathogenesis Primary Secondary Grades How far urine backs up Dx: Abdominal US Voiding Cystourethrogram (VCUG) Radionuclide Cystogram Treatment child Severe

2.2.2. Posterior uretrhal valve aka Congenital Obstructive Posterior urethral membrane Demographs Boys Pathogenesis membranous folds of posterior urethra (closest to bladder) obstruct realeasing of bladder disruption in development bt 9-14 wks in utero Complications Oligohydramnios urine backup Increased Bladder pressure Chornic Kidney Disease Diagnosis US Treatment Surgery and Ablation

2.3. Renal Agenesis

2.3.1. types unilateral Symptoms Complications bilateral Problems start in utero (wk 16) Prognosis

2.3.2. cause uretic bud fails to induce metanephric blastema

2.3.3. pathogenesis genetic factors environmental factors toxins infecitons

2.4. Cystic Kidney Diseases

2.4.1. By Symptom Size Shrunken Hypertrophy Kidneys affected Unilateral Bilateral Location of Cysts Renal Cortex Renal Medulla Parenchyma Corticomedullary jxn Etiology Noninherited Genetic Age Infant Child/Adult

2.4.2. By Disease Mulitcystic Dysplastic Kidney (MCKD) Cause Pathogenesis: Presentation Associated with Treatment Polycystic Kidney Disease 2 Types Symptoms Diagnosis Complications Treatment Medullary Cystic kidney disease Cause Pathogenesis Demo Presentation Complications Findings Dx Treatment: Nephronophthisis Cause Characterized as Demographics Subtypes Pathogenesis Presents with Associated with Complications Findings Dx Treatment: Medullary Sponge Kidney aka Cacchi-Ricci Disease Cause Demo Pathogenesis Presentation Complications Dx Tx

3. Other Causes

3.1. Amniotic Rupture

3.2. Uteroplacenta Insufficiency

3.2.1. low blood flow to placenta

3.3. Atresia of Ureter or Urethra

4. Acute Renal Failure

4.1. Presentation

4.1.1. Acute (within days)

4.1.2. renal failure

4.2. Findings

4.2.1. azotemia

4.2.2. Increased BUN

4.2.3. increased Cr

4.2.4. Often oliguria

4.3. 3 Types

4.3.1. Prerenal Azotemia Pathogenesis decreased blood flow Findings decreased GFR azotemia oliguria BUN:Cr >15 Tubular function is intact

4.3.2. Post Renal Azotemia Pathogenesis block outflow Presentation General Early Stages Chronic

4.3.3. Infrarenal Acute Tubular Necrosis Cause Pathogenesis Finidngs Note Tx Prognosis Dysfunctional Tubular Epithelium Findings Acute Interstitial Nephritis Cause Pathogenesis Presentation Findings Prognosis Renal Pappilary Necrosis Causes Pathogenesis Presentaiton

5. Nephrotic Syndrome

5.1. General

5.1.1. Labs proteinuria (>3.5 g/day) Hypoalbuminemia decreased oncotic pressure Hypogammaglobulinemia Hypercoagulable state due to loss of antitrhombin III Hyperlipidemia Hypercholesterolemia Fatty casts

5.1.2. Symptoms pitting edema Increased risk of infection

5.2. By Diseases

5.2.1. Minimal Change Disease (MCD) Note most common cause of nephrotic disease in children Demo Children Cause idiopathic Pathogenesis cytokines destroy footprocesses Associated with Hodgkin lymphoma Findings Imaging Selective proteinuria Treatment steriods Prognosis if doens't respond, evolves into FSGS

5.2.2. Focal Segmental Glomerulosclerosis (FSGS) Demo Hispanics African Americans Cause idiopathic Associated with HIV herion use sickle cells Findings Imaging IF Tx proor response to steriods Prognosis processes to chronic renal failure

5.2.3. Membranous Nephropathy Demo Caucasian adults Note most common cause of nephrotic syndrome in Caucasian adults Causes Idiopathic Associated with solid tumors Hep B/C SLE non iv drugs Findings Histo Treatment poor response to steriods Prognosis progresses to chronic renal failure

5.2.4. Membranoproliferative Glomerulonephritis Findings H&E IF Pathology mesangial cell proliferates, separating the deposits Immune deposits 2 Types Type I Type II (Dense deposit disease) Treatment Poor response to steriods Prognosis progresses to chronic renal failure Can be nephritic or nephrotic

5.2.5. Diabetes Mellitis Pathophysiology high BGL Findings High GFR microalbuminuria Imaging Prognosis nephrotic syndrome treatment ACE Inhibitors slow progression

5.2.6. Systemic Amyloidosis Pathogenesis Systemic amyloid deposits in the mesangium Prognosis nephrotic syndrome Imaging applegreen birefringence under polarized light using Congo Red Stain

5.3. By Symptom

5.3.1. Population Caucasian Adults Membranous Nephropathy children minimal change disease Hispanics FSGS AA FSGS

5.3.2. By disease HIV FSGS IV Drug Users FSGS Sickle Cell FSGS Hodgekins Lymphoma MCD Hep B/C Membranous Nephropathy Membranoproliferative Glomerulonephritis Type I solid tumors Membranous Nephropathy SLE Membranous Nephropathy drugs (not IV) Membranous Nephropathy Diabetes nephrotic sclerosis of the mesangium

5.3.3. by location of deposits subendo Type I MPGN Sub epi Membranous Glomerulonephropathy in BM Type II MPGN

5.3.4. Imaging H&E Normal Sclerosis thick basement membrane Tram track Kimmelstiel-Wilson nodules EM effacement of foot processes Spike and Dome appearance IF neg Granular applegreen birefringence under polarized light

5.3.5. Key Problem Effacement of foot processes MCD FSGS Deposition of immune complexes Membranonous Nephropathy Membranoproliferative Glomerulonephritis Systemic DM Systemic Amyloidosis

5.3.6. Treatment Steroids Responds well Doesn't respond well ACE inhibitors Diabetes Mellitis

5.4. Pearls

5.4.1. C3 nephritic factor Membranoproliferative Glomerulonephritis`

6. Nephritic Syndrome

6.1. General

6.1.1. Characterized by Glomerular inflammation glomerular bleeding

6.1.2. Findings Limited proteinuria (<3.5 g/day) oliguria azotemia salt retention periorbital edema HTN RBC casts dysmorphic RBC in urine Biopsy hypercellular, inflamed glomeruli

6.1.3. Pathophys Immune complex deposition acitvates complement

6.2. By Findings

6.2.1. Post Infection PSGN sore throat impetigo Berger mucosal infection

6.2.2. Demo kids post infection PSGN SLE Rapidly Progressive Glomerulonephritis (Diffuse proliferative glomerulonephritis

6.2.3. Key Words Cola-colored urine PSGN

6.2.4. Imaging H&E Hypercellular, inflamed glomeruli Cresents (made of Fibrin and macs) EM subepithelial humps IF Granular Linear Negative IF (pauci-immune) IgA immune complex deposition in the mesangium

6.2.5. Labs ANCA p-ANCA c-ANCA

6.3. Diseases

6.3.1. Post Streptococcal Glomerulonephritis Cause group A B-hemolytic strep infection or post other infection Demo mostly children Presentation 2-3 weeks post infection hematuria cola-colored urine oliguria HTN periorbital edema Findings Imaging Treatment Supportive Prognosis Kids Adults

6.3.2. Rapidly Progressive Glomulonephritis General progresses to renal failure in weeks to months Findings Etiologies Findings

6.3.3. IgA Nephropathy (Berger Diz) Pathophys IgA complex deposition in mesangium post mucosal infeciton note- most common nephropathy worldwide Demo Child Findings Hematuria w/ RBC casts Imaging Prognosis renal failure may resolve

6.3.4. Alport Syndrome Pathophys defect in Type IV collagen Cause inherited Findings hematuria sensory hearing loss ocular disturbances

7. UTIs

7.1. General

7.1.1. MCC ascending infenction

7.1.2. Demo more female>male

7.1.3. Risk factors sex urinary stasis catheters

7.2. Diseases

7.2.1. Cystitis Pathophys Infection of the bladder Findings UA Dipstick culture If pyuria w/ negative urine culture (sterile pyuria) Presentation dysuria frequency urgency suprapubic pain Etiology E.Coli 80% Staph Sap Klebsiella pneumonia Proteus mirabilis Enterococcus faecalis

7.2.2. Pyelonephritis Patho infection of the kidney Presentation Fever (systemic signs) Flank pain WBC casts leukocytosis cystitis symptoms Etiology E Coli (90%) Enterococcus Faecalis Klebsiella

7.2.3. Chronic Pyelonephritis patho multiple abouts of acute pyelophritis etiology Kids Adults Findings Cortical scarring blunted calyxes scarring at upper and lower poles thyroidization waxy casts

7.3. by Findings

8. Nephrolithiasis

8.1. Kidney Stones

8.1.1. Types Calcium Caused by/risk factors Imaging Calcium Oxalate Calcium Phosphate Struvite aka: Magnesium Ammonium Phosphate Stones Caused by Shape Treatment Imaging: Uric Acid Caused by Associated with Shape Imaging Treatment: Cystein Caused by Findings Shape

8.1.2. Shapes hexagonal Cystine envelope Calcium oxalate wedge-shaped prism Calcium Phosphate Rhomboid or rosettes Uric Acid dumbell Calcium Oxalate coffin lid Struvite

8.1.3. Presents with unilateral flank tenderness colicky pain radiating to goin hematuria Obstruction s

8.1.4. treatment fluid intake plus situation Thiazide citrate urine alkalinization etc

9. Chronic Renal Failure aka ESKD

9.1. caused by

9.1.1. glomuular probs

9.1.2. tubular probs

9.1.3. inflammatory probs

9.1.4. vascular probs

9.2. Etiologies

9.2.1. DM

9.2.2. HTN

9.2.3. Glomerular disease

9.3. Findings

9.3.1. Uremia/Azotemia nausea anorexia pericarditis plt dysfucntion encephalopathy with asterixis deposition of urea cyrstals in skin

9.3.2. Salt and water retention HTN

9.3.3. Hyper kalemia metabolic acidosis icnreased anion gap

9.3.4. decreased EPO anemia

9.3.5. Hypocalcemia decreased 1-a-hydroxylatio of Vit D by PCT Hyperphostatemia

9.3.6. Renal osteodystrophy secondary hyperparathyroidism osteomalacia don't have calcium to solidify phosphtte crystalsa nd make bone osteoporiss leech from bone b/c metabolic acidosis osteitis fibrosa cystica break down bone to make up for Ca

9.4. treatment

9.4.1. dialysis

9.4.2. transplant

9.5. complications

9.5.1. dialsysis cysts shrunken kidneys increasing change of renal cell carcinoma

10. Renal Neoplasia

10.1. Angiomyolipoma

10.1.1. Patho Hamartoma blood vessels smooth muscle adipose tissue

10.1.2. Associations Tuberous sclerosis

10.2. Renal Cell Carcinoma

10.2.1. Pathophys Malignant epithelial tumor from kidney tubules

10.2.2. Pathogenesis genetic AD

10.2.3. Presentation Triad triad doesn't typically occur together Hematuria palpable mass flank pain fever weight loss paraneoplastic syndrome increase in Left-sided varicocele blockage of drainage of L spermatic cord Sporadic Upper pole of kidney

10.2.4. 2 Etiologies Hereditary Demo Presentaiton Sporadic demo: presentation: risk factor:

10.2.5. Findings gross yello mass microscoppic clear cytoplasm

10.2.6. Staging T based on size and involvement of the renal veins loves to go to vein N spread to retroperitoneal lymph nodes

10.3. Wilm's Tumor

10.3.1. Note: most common malignant renal tumor in children

10.3.2. Demo Children avg age =3

10.3.3. Pathophys malignant tumor made of Blastema primitive glomeruli primitive tubules stromal cells

10.3.4. presentaiton large flank mass unilateral hematuria HTN secondary to renin secretion

10.3.5. Etiology Sporadic 90% WAGR syndrome Densy-Drash syndrome Beckwith-Wiedemann syndrome

11. Lower Urinary tract Carcinoma

11.1. Urothelial (Transitional Cell) Carcinoma

11.1.1. arises from urothelial lining of renal pelvis ureter bladder urethra

11.1.2. pathophys malignant often mutifocal recur "field defect" most common in bladder

11.1.3. note: most common type of lower urinary tract cancer

11.1.4. risk factor smoking naphthylamine in cig smoke azo dyes (hair dyes) long term drug use cyclophosphamide phenacetic

11.1.5. demo older adults

11.1.6. presentation painless hematuria

11.1.7. Etiology 2 pathways Flat Papillary

11.2. Squamous Cell Carcinoma

11.2.1. Patho Malignant squamous cells mc with bladder starts with metaplasia to squamous (from transitional) then becomes dysplastic

11.2.2. risk factors chronic cystitis Schisto long-standing nephrolithiasis

11.2.3. demo odler woman Egyptian male

11.3. Adenocarcinoma

11.3.1. Patho malignant prolif of glands usually bladder

11.3.2. Etiology from urachal remnant develops at dome of bladder cystitis glandularis columnar hyperplasia exstrophy congenital failure to form the caudal portion of the ant abd and bladder walls