Kidney Pathology

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Kidney Pathology por Mind Map: Kidney Pathology

1. Hydronephrosis

1.1. Causes

1.1.1. Obstruction

1.1.2. Compression

1.2. Who

1.2.1. fetus

1.2.1.1. cause unknown

1.2.1.2. often resolves

1.2.2. Third Trimester

1.2.2.1. vesicouretal reflex

1.2.2.1.1. retrograde flow of urine from bladder into urinary tract

1.2.2.2. congenital uretopelvic obstruction

1.2.2.2.1. problem/blockage of urine leaving renal pelvis

1.2.3. young child

1.2.3.1. Congentital malformations

1.2.3.1.1. uretoerocele

1.2.3.1.2. posterior urethral valves

1.2.4. Adults

1.2.4.1. Acquired Disease

1.2.4.1.1. Kidney Stones

1.2.4.1.2. BPH

1.3. Presents with

1.3.1. Obstructive

1.3.1.1. Flank Pain

1.3.1.2. Groin Pain

1.3.1.3. UTI

1.3.2. Hydronephrosis

1.3.2.1. post renal azotemia

1.3.2.1.1. 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

1.5.1.1. acute

1.5.1.1.1. nephrostomy tube

1.5.1.2. Chronic

1.5.1.2.1. Ureteric stent

1.5.1.2.2. Pyeloplasty

1.5.1.3. Lower obstruction

1.5.1.3.1. Urinary catheter

1.5.1.3.2. Suprapubic catheter

2. Congenital

2.1. Horshoe Kidney

2.1.1. How

2.1.1.1. 1- Mechanical Fusion

2.1.1.1.1. at 5 wks (metanephros)

2.1.1.1.2. flexion pushes kidneys together

2.1.1.1.3. inferior poles touch and fuse

2.1.1.1.4. leads to isthmus

2.1.1.2. 2-Teratogenic event

2.1.1.2.1. Posterior Nephrogenic cells migrate to posterior pole of kidney (wrong spot)

2.1.1.2.2. leads to isthmus

2.1.2. Complications

2.1.2.1. Stuck on Inferior mesenteric artery on ascention

2.1.2.2. leads to lower placement

2.1.2.3. can cause compression of kidney

2.1.2.4. can cause hydropnephrosis

2.1.3. associations

2.1.3.1. Kidney stones

2.1.3.2. Infection

2.1.3.3. Chromosomal Disorders

2.1.3.3.1. Turner

2.1.3.3.2. Trisomies 13,18,21

2.1.3.4. increased risk of

2.1.3.4.1. kidney cancer

2.1.4. Demographics

2.1.4.1. common

2.1.4.1.1. 1:500

2.1.4.2. men>women

2.1.5. Symptoms

2.1.5.1. normally asymptomatic

2.1.6. Tx

2.1.6.1. normally not necessary

2.1.6.2. might need sx if leads to complication

2.2. Obstructive (see Hydronephrosis)

2.2.1. Primary Vesicouretal Reflux

2.2.1.1. Notes

2.2.1.1.1. Most common

2.2.1.2. Pathogenesis

2.2.1.2.1. Primary

2.2.1.2.2. Secondary

2.2.1.3. Grades

2.2.1.3.1. How far urine backs up

2.2.1.4. Dx:

2.2.1.4.1. Abdominal US

2.2.1.4.2. Voiding Cystourethrogram (VCUG)

2.2.1.4.3. Radionuclide Cystogram

2.2.1.5. Treatment

2.2.1.5.1. child

2.2.1.5.2. Severe

2.2.2. Posterior uretrhal valve aka Congenital Obstructive Posterior urethral membrane

2.2.2.1. Demographs

2.2.2.1.1. Boys

2.2.2.2. Pathogenesis

2.2.2.2.1. membranous folds of posterior urethra (closest to bladder) obstruct realeasing of bladder

2.2.2.2.2. disruption in development bt 9-14 wks in utero

2.2.2.3. Complications

2.2.2.3.1. Oligohydramnios

2.2.2.3.2. urine backup

2.2.2.3.3. Increased Bladder pressure

2.2.2.3.4. Chornic Kidney Disease

2.2.2.4. Diagnosis

2.2.2.4.1. US

2.2.2.5. Treatment

2.2.2.5.1. Surgery and Ablation

2.3. Renal Agenesis

2.3.1. types

2.3.1.1. unilateral

2.3.1.1.1. Symptoms

2.3.1.1.2. Complications

2.3.1.2. bilateral

2.3.1.2.1. Problems start in utero (wk 16)

2.3.1.2.2. Prognosis

2.3.2. cause

2.3.2.1. uretic bud fails to induce metanephric blastema

2.3.3. pathogenesis

2.3.3.1. genetic factors

2.3.3.2. environmental factors

2.3.3.2.1. toxins

2.3.3.2.2. infecitons

2.4. Cystic Kidney Diseases

2.4.1. By Symptom

2.4.1.1. Size

2.4.1.1.1. Shrunken

2.4.1.1.2. Hypertrophy

2.4.1.2. Kidneys affected

2.4.1.2.1. Unilateral

2.4.1.2.2. Bilateral

2.4.1.3. Location of Cysts

2.4.1.3.1. Renal Cortex

2.4.1.3.2. Renal Medulla

2.4.1.3.3. Parenchyma

2.4.1.3.4. Corticomedullary jxn

2.4.1.4. Etiology

2.4.1.4.1. Noninherited

2.4.1.4.2. Genetic

2.4.1.5. Age

2.4.1.5.1. Infant

2.4.1.5.2. Child/Adult

2.4.2. By Disease

2.4.2.1. Mulitcystic Dysplastic Kidney (MCKD)

2.4.2.1.1. Cause

2.4.2.1.2. Pathogenesis:

2.4.2.1.3. Presentation

2.4.2.1.4. Associated with

2.4.2.1.5. Treatment

2.4.2.2. Polycystic Kidney Disease

2.4.2.2.1. 2 Types

2.4.2.2.2. Symptoms

2.4.2.2.3. Diagnosis

2.4.2.2.4. Complications

2.4.2.2.5. Treatment

2.4.2.3. Medullary Cystic kidney disease

2.4.2.3.1. Cause

2.4.2.3.2. Pathogenesis

2.4.2.3.3. Demo

2.4.2.3.4. Presentation

2.4.2.3.5. Complications

2.4.2.3.6. Findings

2.4.2.3.7. Dx

2.4.2.3.8. Treatment:

2.4.2.4. Nephronophthisis

2.4.2.4.1. Cause

2.4.2.4.2. Characterized as

2.4.2.4.3. Demographics

2.4.2.4.4. Subtypes

2.4.2.4.5. Pathogenesis

2.4.2.4.6. Presents with

2.4.2.4.7. Associated with

2.4.2.4.8. Complications

2.4.2.4.9. Findings

2.4.2.4.10. Dx

2.4.2.4.11. Treatment:

2.4.2.5. Medullary Sponge Kidney

2.4.2.5.1. aka Cacchi-Ricci Disease

2.4.2.5.2. Cause

2.4.2.5.3. Demo

2.4.2.5.4. Pathogenesis

2.4.2.5.5. Presentation

2.4.2.5.6. Complications

2.4.2.5.7. Dx

2.4.2.5.8. 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

4.3.1.1. Pathogenesis

4.3.1.1.1. decreased blood flow

4.3.1.2. Findings

4.3.1.2.1. decreased GFR

4.3.1.2.2. azotemia

4.3.1.2.3. oliguria

4.3.1.2.4. BUN:Cr >15

4.3.1.2.5. Tubular function is intact

4.3.2. Post Renal Azotemia

4.3.2.1. Pathogenesis

4.3.2.1.1. block outflow

4.3.2.2. Presentation

4.3.2.2.1. General

4.3.2.2.2. Early Stages

4.3.2.2.3. Chronic

4.3.3. Infrarenal

4.3.3.1. Acute Tubular Necrosis

4.3.3.1.1. Cause

4.3.3.1.2. Pathogenesis

4.3.3.1.3. Finidngs

4.3.3.1.4. Note

4.3.3.1.5. Tx

4.3.3.1.6. Prognosis

4.3.3.2. Dysfunctional Tubular Epithelium

4.3.3.2.1. Findings

4.3.3.3. Acute Interstitial Nephritis

4.3.3.3.1. Cause

4.3.3.3.2. Pathogenesis

4.3.3.3.3. Presentation

4.3.3.3.4. Findings

4.3.3.3.5. Prognosis

4.3.3.4. Renal Pappilary Necrosis

4.3.3.4.1. Causes

4.3.3.4.2. Pathogenesis

4.3.3.4.3. Presentaiton

5. Nephrotic Syndrome

5.1. General

5.1.1. Labs

5.1.1.1. proteinuria (>3.5 g/day)

5.1.1.2. Hypoalbuminemia

5.1.1.2.1. decreased oncotic pressure

5.1.1.3. Hypogammaglobulinemia

5.1.1.4. Hypercoagulable state

5.1.1.4.1. due to loss of antitrhombin III

5.1.1.5. Hyperlipidemia

5.1.1.6. Hypercholesterolemia

5.1.1.7. Fatty casts

5.1.2. Symptoms

5.1.2.1. pitting edema

5.1.2.2. Increased risk of infection

5.2. By Diseases

5.2.1. Minimal Change Disease (MCD)

5.2.1.1. Note

5.2.1.1.1. most common cause of nephrotic disease in children

5.2.1.2. Demo

5.2.1.2.1. Children

5.2.1.3. Cause

5.2.1.3.1. idiopathic

5.2.1.4. Pathogenesis

5.2.1.4.1. cytokines destroy footprocesses

5.2.1.5. Associated with

5.2.1.5.1. Hodgkin lymphoma

5.2.1.6. Findings

5.2.1.6.1. Imaging

5.2.1.6.2. Selective proteinuria

5.2.1.7. Treatment

5.2.1.7.1. steriods

5.2.1.8. Prognosis

5.2.1.8.1. if doens't respond, evolves into FSGS

5.2.2. Focal Segmental Glomerulosclerosis (FSGS)

5.2.2.1. Demo

5.2.2.1.1. Hispanics

5.2.2.1.2. African Americans

5.2.2.2. Cause

5.2.2.2.1. idiopathic

5.2.2.3. Associated with

5.2.2.3.1. HIV

5.2.2.3.2. herion use

5.2.2.3.3. sickle cells

5.2.2.4. Findings

5.2.2.4.1. Imaging

5.2.2.4.2. IF

5.2.2.5. Tx

5.2.2.5.1. proor response to steriods

5.2.2.6. Prognosis

5.2.2.6.1. processes to chronic renal failure

5.2.3. Membranous Nephropathy

5.2.3.1. Demo

5.2.3.1.1. Caucasian adults

5.2.3.2. Note

5.2.3.2.1. most common cause of nephrotic syndrome in Caucasian adults

5.2.3.3. Causes

5.2.3.3.1. Idiopathic

5.2.3.4. Associated with

5.2.3.4.1. solid tumors

5.2.3.4.2. Hep B/C

5.2.3.4.3. SLE

5.2.3.4.4. non iv drugs

5.2.3.5. Findings

5.2.3.5.1. Histo

5.2.3.6. Treatment

5.2.3.6.1. poor response to steriods

5.2.3.7. Prognosis

5.2.3.7.1. progresses to chronic renal failure

5.2.4. Membranoproliferative Glomerulonephritis

5.2.4.1. Findings

5.2.4.1.1. H&E

5.2.4.1.2. IF

5.2.4.2. Pathology

5.2.4.2.1. mesangial cell proliferates, separating the deposits

5.2.4.2.2. Immune deposits

5.2.4.3. 2 Types

5.2.4.3.1. Type I

5.2.4.3.2. Type II (Dense deposit disease)

5.2.4.4. Treatment

5.2.4.4.1. Poor response to steriods

5.2.4.5. Prognosis

5.2.4.5.1. progresses to chronic renal failure

5.2.4.5.2. Can be nephritic or nephrotic

5.2.5. Diabetes Mellitis

5.2.5.1. Pathophysiology

5.2.5.1.1. high BGL

5.2.5.2. Findings

5.2.5.2.1. High GFR

5.2.5.2.2. microalbuminuria

5.2.5.2.3. Imaging

5.2.5.3. Prognosis

5.2.5.3.1. nephrotic syndrome

5.2.5.4. treatment

5.2.5.4.1. ACE Inhibitors slow progression

5.2.6. Systemic Amyloidosis

5.2.6.1. Pathogenesis

5.2.6.1.1. Systemic

5.2.6.1.2. amyloid deposits in the mesangium

5.2.6.2. Prognosis

5.2.6.2.1. nephrotic syndrome

5.2.6.3. Imaging

5.2.6.3.1. applegreen birefringence under polarized light

5.2.6.3.2. using Congo Red Stain

5.3. By Symptom

5.3.1. Population

5.3.1.1. Caucasian Adults

5.3.1.1.1. Membranous Nephropathy

5.3.1.2. children

5.3.1.2.1. minimal change disease

5.3.1.3. Hispanics

5.3.1.3.1. FSGS

5.3.1.4. AA

5.3.1.4.1. FSGS

5.3.2. By disease

5.3.2.1. HIV

5.3.2.1.1. FSGS

5.3.2.2. IV Drug Users

5.3.2.2.1. FSGS

5.3.2.3. Sickle Cell

5.3.2.3.1. FSGS

5.3.2.4. Hodgekins Lymphoma

5.3.2.4.1. MCD

5.3.2.5. Hep B/C

5.3.2.5.1. Membranous Nephropathy

5.3.2.5.2. Membranoproliferative Glomerulonephritis Type I

5.3.2.6. solid tumors

5.3.2.6.1. Membranous Nephropathy

5.3.2.7. SLE

5.3.2.7.1. Membranous Nephropathy

5.3.2.8. drugs (not IV)

5.3.2.8.1. Membranous Nephropathy

5.3.2.9. Diabetes

5.3.2.9.1. nephrotic sclerosis of the mesangium

5.3.3. by location of deposits

5.3.3.1. subendo

5.3.3.1.1. Type I MPGN

5.3.3.2. Sub epi

5.3.3.2.1. Membranous Glomerulonephropathy

5.3.3.3. in BM

5.3.3.3.1. Type II MPGN

5.3.4. Imaging

5.3.4.1. H&E

5.3.4.1.1. Normal

5.3.4.1.2. Sclerosis

5.3.4.1.3. thick basement membrane

5.3.4.1.4. Tram track

5.3.4.1.5. Kimmelstiel-Wilson nodules

5.3.4.2. EM

5.3.4.2.1. effacement of foot processes

5.3.4.2.2. Spike and Dome appearance

5.3.4.3. IF

5.3.4.3.1. neg

5.3.4.3.2. Granular

5.3.4.3.3. applegreen birefringence under polarized light

5.3.5. Key Problem

5.3.5.1. Effacement of foot processes

5.3.5.1.1. MCD

5.3.5.1.2. FSGS

5.3.5.2. Deposition of immune complexes

5.3.5.2.1. Membranonous Nephropathy

5.3.5.2.2. Membranoproliferative Glomerulonephritis

5.3.5.3. Systemic

5.3.5.3.1. DM

5.3.5.3.2. Systemic Amyloidosis

5.3.6. Treatment

5.3.6.1. Steroids

5.3.6.1.1. Responds well

5.3.6.1.2. Doesn't respond well

5.3.6.2. ACE inhibitors

5.3.6.2.1. Diabetes Mellitis

5.4. Pearls

5.4.1. C3 nephritic factor

5.4.1.1. Membranoproliferative Glomerulonephritis`

6. Nephritic Syndrome

6.1. General

6.1.1. Characterized by

6.1.1.1. Glomerular inflammation

6.1.1.2. glomerular bleeding

6.1.2. Findings

6.1.2.1. Limited proteinuria (<3.5 g/day)

6.1.2.2. oliguria

6.1.2.3. azotemia

6.1.2.4. salt retention

6.1.2.4.1. periorbital edema

6.1.2.4.2. HTN

6.1.2.5. RBC casts

6.1.2.6. dysmorphic RBC in urine

6.1.2.7. Biopsy

6.1.2.7.1. hypercellular, inflamed glomeruli

6.1.3. Pathophys

6.1.3.1. Immune complex deposition

6.1.3.1.1. acitvates complement

6.2. By Findings

6.2.1. Post Infection

6.2.1.1. PSGN

6.2.1.1.1. sore throat

6.2.1.1.2. impetigo

6.2.1.2. Berger

6.2.1.2.1. mucosal infection

6.2.2. Demo

6.2.2.1. kids post infection

6.2.2.1.1. PSGN

6.2.2.2. SLE

6.2.2.2.1. Rapidly Progressive Glomerulonephritis (Diffuse proliferative glomerulonephritis

6.2.3. Key Words

6.2.3.1. Cola-colored urine

6.2.3.1.1. PSGN

6.2.4. Imaging

6.2.4.1. H&E

6.2.4.1.1. Hypercellular, inflamed glomeruli

6.2.4.1.2. Cresents (made of Fibrin and macs)

6.2.4.2. EM

6.2.4.2.1. subepithelial humps

6.2.4.3. IF

6.2.4.3.1. Granular

6.2.4.3.2. Linear

6.2.4.3.3. Negative IF (pauci-immune)

6.2.4.3.4. IgA immune complex deposition in the mesangium

6.2.5. Labs

6.2.5.1. ANCA

6.2.5.1.1. p-ANCA

6.2.5.1.2. c-ANCA

6.3. Diseases

6.3.1. Post Streptococcal Glomerulonephritis

6.3.1.1. Cause

6.3.1.1.1. group A B-hemolytic strep infection

6.3.1.1.2. or post other infection

6.3.1.2. Demo

6.3.1.2.1. mostly children

6.3.1.3. Presentation

6.3.1.3.1. 2-3 weeks post infection

6.3.1.3.2. hematuria

6.3.1.3.3. cola-colored urine

6.3.1.3.4. oliguria

6.3.1.3.5. HTN

6.3.1.3.6. periorbital edema

6.3.1.4. Findings

6.3.1.4.1. Imaging

6.3.1.5. Treatment

6.3.1.5.1. Supportive

6.3.1.6. Prognosis

6.3.1.6.1. Kids

6.3.1.6.2. Adults

6.3.2. Rapidly Progressive Glomulonephritis

6.3.2.1. General

6.3.2.1.1. progresses to renal failure in weeks to months

6.3.2.1.2. Findings

6.3.2.2. Etiologies

6.3.2.2.1. Findings

6.3.3. IgA Nephropathy (Berger Diz)

6.3.3.1. Pathophys

6.3.3.1.1. IgA complex deposition in mesangium

6.3.3.1.2. post mucosal infeciton

6.3.3.2. note-

6.3.3.2.1. most common nephropathy worldwide

6.3.3.3. Demo

6.3.3.3.1. Child

6.3.3.4. Findings

6.3.3.4.1. Hematuria w/ RBC casts

6.3.3.4.2. Imaging

6.3.3.5. Prognosis

6.3.3.5.1. renal failure

6.3.3.5.2. may resolve

6.3.4. Alport Syndrome

6.3.4.1. Pathophys

6.3.4.1.1. defect in Type IV collagen

6.3.4.2. Cause

6.3.4.2.1. inherited

6.3.4.3. Findings

6.3.4.3.1. hematuria

6.3.4.3.2. sensory hearing loss

6.3.4.3.3. ocular disturbances

7. UTIs

7.1. General

7.1.1. MCC

7.1.1.1. ascending infenction

7.1.2. Demo

7.1.2.1. more female>male

7.1.3. Risk factors

7.1.3.1. sex

7.1.3.2. urinary stasis

7.1.3.3. catheters

7.2. Diseases

7.2.1. Cystitis

7.2.1.1. Pathophys

7.2.1.1.1. Infection of the bladder

7.2.1.2. Findings

7.2.1.2.1. UA

7.2.1.2.2. Dipstick

7.2.1.2.3. culture

7.2.1.2.4. If pyuria w/ negative urine culture (sterile pyuria)

7.2.1.3. Presentation

7.2.1.3.1. dysuria

7.2.1.3.2. frequency

7.2.1.3.3. urgency

7.2.1.3.4. suprapubic pain

7.2.1.4. Etiology

7.2.1.4.1. E.Coli 80%

7.2.1.4.2. Staph Sap

7.2.1.4.3. Klebsiella pneumonia

7.2.1.4.4. Proteus mirabilis

7.2.1.4.5. Enterococcus faecalis

7.2.2. Pyelonephritis

7.2.2.1. Patho

7.2.2.1.1. infection of the kidney

7.2.2.2. Presentation

7.2.2.2.1. Fever (systemic signs)

7.2.2.2.2. Flank pain

7.2.2.2.3. WBC casts

7.2.2.2.4. leukocytosis

7.2.2.2.5. cystitis symptoms

7.2.2.3. Etiology

7.2.2.3.1. E Coli (90%)

7.2.2.3.2. Enterococcus Faecalis

7.2.2.3.3. Klebsiella

7.2.3. Chronic Pyelonephritis

7.2.3.1. patho

7.2.3.1.1. multiple abouts of acute pyelophritis

7.2.3.2. etiology

7.2.3.2.1. Kids

7.2.3.2.2. Adults

7.2.3.3. Findings

7.2.3.3.1. Cortical scarring

7.2.3.3.2. blunted calyxes

7.2.3.3.3. scarring at upper and lower poles

7.2.3.3.4. thyroidization

7.2.3.3.5. waxy casts

7.3. by Findings

8. Nephrolithiasis

8.1. Kidney Stones

8.1.1. Types

8.1.1.1. Calcium

8.1.1.1.1. Caused by/risk factors

8.1.1.1.2. Imaging

8.1.1.1.3. Calcium Oxalate

8.1.1.1.4. Calcium Phosphate

8.1.1.2. Struvite

8.1.1.2.1. aka: Magnesium Ammonium Phosphate Stones

8.1.1.2.2. Caused by

8.1.1.2.3. Shape

8.1.1.2.4. Treatment

8.1.1.2.5. Imaging:

8.1.1.3. Uric Acid

8.1.1.3.1. Caused by

8.1.1.3.2. Associated with

8.1.1.3.3. Shape

8.1.1.3.4. Imaging

8.1.1.3.5. Treatment:

8.1.1.4. Cystein

8.1.1.4.1. Caused by

8.1.1.4.2. Findings

8.1.1.4.3. Shape

8.1.2. Shapes

8.1.2.1. hexagonal

8.1.2.1.1. Cystine

8.1.2.2. envelope

8.1.2.2.1. Calcium oxalate

8.1.2.3. wedge-shaped prism

8.1.2.3.1. Calcium Phosphate

8.1.2.4. Rhomboid or rosettes

8.1.2.4.1. Uric Acid

8.1.2.5. dumbell

8.1.2.5.1. Calcium Oxalate

8.1.2.6. coffin lid

8.1.2.6.1. Struvite

8.1.3. Presents with

8.1.3.1. unilateral flank tenderness

8.1.3.2. colicky pain radiating to goin

8.1.3.3. hematuria

8.1.3.4. Obstruction s

8.1.4. treatment

8.1.4.1. fluid intake

8.1.4.2. plus situation

8.1.4.2.1. Thiazide

8.1.4.2.2. citrate

8.1.4.2.3. 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

9.3.1.1. nausea

9.3.1.2. anorexia

9.3.1.3. pericarditis

9.3.1.4. plt dysfucntion

9.3.1.5. encephalopathy with asterixis

9.3.1.6. deposition of urea cyrstals in skin

9.3.2. Salt and water retention

9.3.2.1. HTN

9.3.3. Hyper kalemia

9.3.3.1. metabolic acidosis

9.3.3.1.1. icnreased anion gap

9.3.4. decreased EPO

9.3.4.1. anemia

9.3.5. Hypocalcemia

9.3.5.1. decreased 1-a-hydroxylatio of Vit D by PCT

9.3.5.2. Hyperphostatemia

9.3.6. Renal osteodystrophy

9.3.6.1. secondary hyperparathyroidism

9.3.6.2. osteomalacia

9.3.6.2.1. don't have calcium to solidify phosphtte crystalsa nd make bone

9.3.6.3. osteoporiss

9.3.6.3.1. leech from bone b/c metabolic acidosis

9.3.6.4. osteitis fibrosa cystica

9.3.6.4.1. 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

9.5.1.1. cysts

9.5.1.2. shrunken kidneys

9.5.1.3. increasing change of renal cell carcinoma

10. Renal Neoplasia

10.1. Angiomyolipoma

10.1.1. Patho

10.1.1.1. Hamartoma

10.1.1.1.1. blood vessels

10.1.1.1.2. smooth muscle

10.1.1.1.3. adipose tissue

10.1.2. Associations

10.1.2.1. Tuberous sclerosis

10.2. Renal Cell Carcinoma

10.2.1. Pathophys

10.2.1.1. Malignant

10.2.1.2. epithelial tumor

10.2.1.3. from kidney tubules

10.2.2. Pathogenesis

10.2.2.1. genetic

10.2.2.1.1. AD

10.2.3. Presentation

10.2.3.1. Triad

10.2.3.1.1. triad doesn't typically occur together

10.2.3.1.2. Hematuria

10.2.3.1.3. palpable mass

10.2.3.1.4. flank pain

10.2.3.2. fever

10.2.3.3. weight loss

10.2.3.4. paraneoplastic syndrome

10.2.3.4.1. increase in

10.2.3.5. Left-sided varicocele

10.2.3.5.1. blockage of drainage of L spermatic cord

10.2.3.6. Sporadic

10.2.3.6.1. Upper pole of kidney

10.2.4. 2 Etiologies

10.2.4.1. Hereditary

10.2.4.1.1. Demo

10.2.4.1.2. Presentaiton

10.2.4.2. Sporadic

10.2.4.2.1. demo:

10.2.4.2.2. presentation:

10.2.4.2.3. risk factor:

10.2.5. Findings

10.2.5.1. gross yello mass

10.2.5.2. microscoppic clear cytoplasm

10.2.6. Staging

10.2.6.1. T

10.2.6.1.1. based on size and involvement of the renal veins

10.2.6.1.2. loves to go to vein

10.2.6.2. N

10.2.6.2.1. spread to retroperitoneal lymph nodes

10.3. Wilm's Tumor

10.3.1. Note:

10.3.1.1. most common malignant renal tumor in children

10.3.2. Demo

10.3.2.1. Children

10.3.2.1.1. avg age =3

10.3.3. Pathophys

10.3.3.1. malignant tumor

10.3.3.2. made of

10.3.3.2.1. Blastema

10.3.3.2.2. primitive glomeruli

10.3.3.2.3. primitive tubules

10.3.3.2.4. stromal cells

10.3.4. presentaiton

10.3.4.1. large flank mass

10.3.4.2. unilateral

10.3.4.3. hematuria

10.3.4.4. HTN

10.3.4.4.1. secondary to renin secretion

10.3.5. Etiology

10.3.5.1. Sporadic 90%

10.3.5.1.1. WAGR syndrome

10.3.5.1.2. Densy-Drash syndrome

10.3.5.1.3. Beckwith-Wiedemann syndrome

11. Lower Urinary tract Carcinoma

11.1. Urothelial (Transitional Cell) Carcinoma

11.1.1. arises from

11.1.1.1. urothelial lining of

11.1.1.1.1. renal pelvis

11.1.1.1.2. ureter

11.1.1.1.3. bladder

11.1.1.1.4. urethra

11.1.2. pathophys

11.1.2.1. malignant

11.1.2.2. often mutifocal

11.1.2.3. recur

11.1.2.4. "field defect"

11.1.2.5. most common in bladder

11.1.3. note:

11.1.3.1. most common type of lower urinary tract cancer

11.1.4. risk factor

11.1.4.1. smoking

11.1.4.2. naphthylamine

11.1.4.2.1. in cig smoke

11.1.4.3. azo dyes (hair dyes)

11.1.4.4. long term drug use

11.1.4.4.1. cyclophosphamide

11.1.4.4.2. phenacetic

11.1.5. demo

11.1.5.1. older adults

11.1.6. presentation

11.1.6.1. painless

11.1.6.2. hematuria

11.1.7. Etiology

11.1.7.1. 2 pathways

11.1.7.1.1. Flat

11.1.7.1.2. Papillary

11.2. Squamous Cell Carcinoma

11.2.1. Patho

11.2.1.1. Malignant

11.2.1.2. squamous cells

11.2.1.3. mc with bladder

11.2.1.4. starts with metaplasia to squamous (from transitional)

11.2.1.4.1. then becomes dysplastic

11.2.2. risk factors

11.2.2.1. chronic cystitis

11.2.2.2. Schisto

11.2.2.3. long-standing nephrolithiasis

11.2.3. demo

11.2.3.1. odler woman

11.2.3.2. Egyptian male

11.3. Adenocarcinoma

11.3.1. Patho

11.3.1.1. malignant

11.3.1.2. prolif of glands

11.3.1.3. usually bladder

11.3.2. Etiology

11.3.2.1. from urachal remnant

11.3.2.1.1. develops at dome of bladder

11.3.2.2. cystitis glandularis

11.3.2.2.1. columnar hyperplasia

11.3.2.3. exstrophy

11.3.2.3.1. congenital failure to form the caudal portion of the ant abd and bladder walls