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