1. Acute Renal Failure
1.1. Presentation
1.1.1. Acute (within days)
1.1.2. renal failure
1.2. Findings
1.2.1. azotemia
1.2.2. Increased BUN
1.2.3. increased Cr
1.2.4. Often oliguria
1.3. 3 Types
1.3.1. Prerenal Azotemia
1.3.1.1. Pathogenesis
1.3.1.1.1. decreased blood flow
1.3.1.2. Findings
1.3.1.2.1. decreased GFR
1.3.1.2.2. azotemia
1.3.1.2.3. oliguria
1.3.1.2.4. BUN:Cr >15
1.3.1.2.5. Tubular function is intact
1.3.2. Post Renal Azotemia
1.3.2.1. Pathogenesis
1.3.2.1.1. block outflow
1.3.2.2. Presentation
1.3.2.2.1. General
1.3.2.2.2. Early Stages
1.3.2.2.3. Chronic
1.3.3. Infrarenal
1.3.3.1. Acute Tubular Necrosis
1.3.3.1.1. Cause
1.3.3.1.2. Pathogenesis
1.3.3.1.3. Finidngs
1.3.3.1.4. Note
1.3.3.1.5. Tx
1.3.3.1.6. Prognosis
1.3.3.2. Dysfunctional Tubular Epithelium
1.3.3.2.1. Findings
1.3.3.3. Acute Interstitial Nephritis
1.3.3.3.1. Cause
1.3.3.3.2. Pathogenesis
1.3.3.3.3. Presentation
1.3.3.3.4. Findings
1.3.3.3.5. Prognosis
1.3.3.4. Renal Pappilary Necrosis
1.3.3.4.1. Causes
1.3.3.4.2. Pathogenesis
1.3.3.4.3. Presentaiton
2. Nephrotic Syndrome
2.1. General
2.1.1. Labs
2.1.1.1. proteinuria (>3.5 g/day)
2.1.1.2. Hypoalbuminemia
2.1.1.2.1. decreased oncotic pressure
2.1.1.3. Hypogammaglobulinemia
2.1.1.4. Hypercoagulable state
2.1.1.4.1. due to loss of antitrhombin III
2.1.1.5. Hyperlipidemia
2.1.1.6. Hypercholesterolemia
2.1.1.7. Fatty casts
2.1.2. Symptoms
2.1.2.1. pitting edema
2.1.2.2. Increased risk of infection
2.2. By Diseases
2.2.1. Minimal Change Disease (MCD)
2.2.1.1. Note
2.2.1.1.1. most common cause of nephrotic disease in children
2.2.1.2. Demo
2.2.1.2.1. Children
2.2.1.3. Cause
2.2.1.3.1. idiopathic
2.2.1.4. Pathogenesis
2.2.1.4.1. cytokines destroy footprocesses
2.2.1.5. Associated with
2.2.1.5.1. Hodgkin lymphoma
2.2.1.6. Findings
2.2.1.6.1. Imaging
2.2.1.6.2. Selective proteinuria
2.2.1.7. Treatment
2.2.1.7.1. steriods
2.2.1.8. Prognosis
2.2.1.8.1. if doens't respond, evolves into FSGS
2.2.2. Focal Segmental Glomerulosclerosis (FSGS)
2.2.2.1. Demo
2.2.2.1.1. Hispanics
2.2.2.1.2. African Americans
2.2.2.2. Cause
2.2.2.2.1. idiopathic
2.2.2.3. Associated with
2.2.2.3.1. HIV
2.2.2.3.2. herion use
2.2.2.3.3. sickle cells
2.2.2.4. Findings
2.2.2.4.1. Imaging
2.2.2.4.2. IF
2.2.2.5. Tx
2.2.2.5.1. proor response to steriods
2.2.2.6. Prognosis
2.2.2.6.1. processes to chronic renal failure
2.2.3. Membranous Nephropathy
2.2.3.1. Demo
2.2.3.1.1. Caucasian adults
2.2.3.2. Note
2.2.3.2.1. most common cause of nephrotic syndrome in Caucasian adults
2.2.3.3. Causes
2.2.3.3.1. Idiopathic
2.2.3.4. Associated with
2.2.3.4.1. solid tumors
2.2.3.4.2. Hep B/C
2.2.3.4.3. SLE
2.2.3.4.4. non iv drugs
2.2.3.5. Findings
2.2.3.5.1. Histo
2.2.3.6. Treatment
2.2.3.6.1. poor response to steriods
2.2.3.7. Prognosis
2.2.3.7.1. progresses to chronic renal failure
2.2.4. Membranoproliferative Glomerulonephritis
2.2.4.1. Findings
2.2.4.1.1. H&E
2.2.4.1.2. IF
2.2.4.2. Pathology
2.2.4.2.1. mesangial cell proliferates, separating the deposits
2.2.4.2.2. Immune deposits
2.2.4.3. 2 Types
2.2.4.3.1. Type I
2.2.4.3.2. Type II (Dense deposit disease)
2.2.4.4. Treatment
2.2.4.4.1. Poor response to steriods
2.2.4.5. Prognosis
2.2.4.5.1. progresses to chronic renal failure
2.2.4.5.2. Can be nephritic or nephrotic
2.2.5. Diabetes Mellitis
2.2.5.1. Pathophysiology
2.2.5.1.1. high BGL
2.2.5.2. Findings
2.2.5.2.1. High GFR
2.2.5.2.2. microalbuminuria
2.2.5.2.3. Imaging
2.2.5.3. Prognosis
2.2.5.3.1. nephrotic syndrome
2.2.5.4. treatment
2.2.5.4.1. ACE Inhibitors slow progression
2.2.6. Systemic Amyloidosis
2.2.6.1. Pathogenesis
2.2.6.1.1. Systemic
2.2.6.1.2. amyloid deposits in the mesangium
2.2.6.2. Prognosis
2.2.6.2.1. nephrotic syndrome
2.2.6.3. Imaging
2.2.6.3.1. applegreen birefringence under polarized light
2.2.6.3.2. using Congo Red Stain
2.3. By Symptom
2.3.1. Population
2.3.1.1. Caucasian Adults
2.3.1.1.1. Membranous Nephropathy
2.3.1.2. children
2.3.1.2.1. minimal change disease
2.3.1.3. Hispanics
2.3.1.3.1. FSGS
2.3.1.4. AA
2.3.1.4.1. FSGS
2.3.2. By disease
2.3.2.1. HIV
2.3.2.1.1. FSGS
2.3.2.2. IV Drug Users
2.3.2.2.1. FSGS
2.3.2.3. Sickle Cell
2.3.2.3.1. FSGS
2.3.2.4. Hodgekins Lymphoma
2.3.2.4.1. MCD
2.3.2.5. Hep B/C
2.3.2.5.1. Membranous Nephropathy
2.3.2.5.2. Membranoproliferative Glomerulonephritis Type I
2.3.2.6. solid tumors
2.3.2.6.1. Membranous Nephropathy
2.3.2.7. SLE
2.3.2.7.1. Membranous Nephropathy
2.3.2.8. drugs (not IV)
2.3.2.8.1. Membranous Nephropathy
2.3.2.9. Diabetes
2.3.2.9.1. nephrotic sclerosis of the mesangium
2.3.3. by location of deposits
2.3.3.1. subendo
2.3.3.1.1. Type I MPGN
2.3.3.2. Sub epi
2.3.3.2.1. Membranous Glomerulonephropathy
2.3.3.3. in BM
2.3.3.3.1. Type II MPGN
2.3.4. Imaging
2.3.4.1. H&E
2.3.4.1.1. Normal
2.3.4.1.2. Sclerosis
2.3.4.1.3. thick basement membrane
2.3.4.1.4. Tram track
2.3.4.1.5. Kimmelstiel-Wilson nodules
2.3.4.2. EM
2.3.4.2.1. effacement of foot processes
2.3.4.2.2. Spike and Dome appearance
2.3.4.3. IF
2.3.4.3.1. neg
2.3.4.3.2. Granular
2.3.4.3.3. applegreen birefringence under polarized light
2.3.5. Key Problem
2.3.5.1. Effacement of foot processes
2.3.5.1.1. MCD
2.3.5.1.2. FSGS
2.3.5.2. Deposition of immune complexes
2.3.5.2.1. Membranonous Nephropathy
2.3.5.2.2. Membranoproliferative Glomerulonephritis
2.3.5.3. Systemic
2.3.5.3.1. DM
2.3.5.3.2. Systemic Amyloidosis
2.3.6. Treatment
2.3.6.1. Steroids
2.3.6.1.1. Responds well
2.3.6.1.2. Doesn't respond well
2.3.6.2. ACE inhibitors
2.3.6.2.1. Diabetes Mellitis
2.4. Pearls
2.4.1. C3 nephritic factor
2.4.1.1. Membranoproliferative Glomerulonephritis`
3. Nephritic Syndrome
3.1. General
3.1.1. Characterized by
3.1.1.1. Glomerular inflammation
3.1.1.2. glomerular bleeding
3.1.2. Findings
3.1.2.1. Limited proteinuria (<3.5 g/day)
3.1.2.2. oliguria
3.1.2.3. azotemia
3.1.2.4. salt retention
3.1.2.4.1. periorbital edema
3.1.2.4.2. HTN
3.1.2.5. RBC casts
3.1.2.6. dysmorphic RBC in urine
3.1.2.7. Biopsy
3.1.2.7.1. hypercellular, inflamed glomeruli
3.1.3. Pathophys
3.1.3.1. Immune complex deposition
3.1.3.1.1. acitvates complement
3.2. By Findings
3.2.1. Post Infection
3.2.1.1. PSGN
3.2.1.1.1. sore throat
3.2.1.1.2. impetigo
3.2.1.2. Berger
3.2.1.2.1. mucosal infection
3.2.2. Demo
3.2.2.1. kids post infection
3.2.2.1.1. PSGN
3.2.2.2. SLE
3.2.2.2.1. Rapidly Progressive Glomerulonephritis (Diffuse proliferative glomerulonephritis
3.2.3. Key Words
3.2.3.1. Cola-colored urine
3.2.3.1.1. PSGN
3.2.4. Imaging
3.2.4.1. H&E
3.2.4.1.1. Hypercellular, inflamed glomeruli
3.2.4.1.2. Cresents (made of Fibrin and macs)
3.2.4.2. EM
3.2.4.2.1. subepithelial humps
3.2.4.3. IF
3.2.4.3.1. Granular
3.2.4.3.2. Linear
3.2.4.3.3. Negative IF (pauci-immune)
3.2.4.3.4. IgA immune complex deposition in the mesangium
3.2.5. Labs
3.2.5.1. ANCA
3.2.5.1.1. p-ANCA
3.2.5.1.2. c-ANCA
3.3. Diseases
3.3.1. Post Streptococcal Glomerulonephritis
3.3.1.1. Cause
3.3.1.1.1. group A B-hemolytic strep infection
3.3.1.1.2. or post other infection
3.3.1.2. Demo
3.3.1.2.1. mostly children
3.3.1.3. Presentation
3.3.1.3.1. 2-3 weeks post infection
3.3.1.3.2. hematuria
3.3.1.3.3. cola-colored urine
3.3.1.3.4. oliguria
3.3.1.3.5. HTN
3.3.1.3.6. periorbital edema
3.3.1.4. Findings
3.3.1.4.1. Imaging
3.3.1.5. Treatment
3.3.1.5.1. Supportive
3.3.1.6. Prognosis
3.3.1.6.1. Kids
3.3.1.6.2. Adults
3.3.2. Rapidly Progressive Glomulonephritis
3.3.2.1. General
3.3.2.1.1. progresses to renal failure in weeks to months
3.3.2.1.2. Findings
3.3.2.2. Etiologies
3.3.2.2.1. Findings
3.3.3. IgA Nephropathy (Berger Diz)
3.3.3.1. Pathophys
3.3.3.1.1. IgA complex deposition in mesangium
3.3.3.1.2. post mucosal infeciton
3.3.3.2. note-
3.3.3.2.1. most common nephropathy worldwide
3.3.3.3. Demo
3.3.3.3.1. Child
3.3.3.4. Findings
3.3.3.4.1. Hematuria w/ RBC casts
3.3.3.4.2. Imaging
3.3.3.5. Prognosis
3.3.3.5.1. renal failure
3.3.3.5.2. may resolve
3.3.4. Alport Syndrome
3.3.4.1. Pathophys
3.3.4.1.1. defect in Type IV collagen
3.3.4.2. Cause
3.3.4.2.1. inherited
3.3.4.3. Findings
3.3.4.3.1. hematuria
3.3.4.3.2. sensory hearing loss
3.3.4.3.3. ocular disturbances
4. UTIs
4.1. General
4.1.1. MCC
4.1.1.1. ascending infenction
4.1.2. Demo
4.1.2.1. more female>male
4.1.3. Risk factors
4.1.3.1. sex
4.1.3.2. urinary stasis
4.1.3.3. catheters
4.2. Diseases
4.2.1. Cystitis
4.2.1.1. Pathophys
4.2.1.1.1. Infection of the bladder
4.2.1.2. Findings
4.2.1.2.1. UA
4.2.1.2.2. Dipstick
4.2.1.2.3. culture
4.2.1.2.4. If pyuria w/ negative urine culture (sterile pyuria)
4.2.1.3. Presentation
4.2.1.3.1. dysuria
4.2.1.3.2. frequency
4.2.1.3.3. urgency
4.2.1.3.4. suprapubic pain
4.2.1.4. Etiology
4.2.1.4.1. E.Coli 80%
4.2.1.4.2. Staph Sap
4.2.1.4.3. Klebsiella pneumonia
4.2.1.4.4. Proteus mirabilis
4.2.1.4.5. Enterococcus faecalis
4.2.2. Pyelonephritis
4.2.2.1. Patho
4.2.2.1.1. infection of the kidney
4.2.2.2. Presentation
4.2.2.2.1. Fever (systemic signs)
4.2.2.2.2. Flank pain
4.2.2.2.3. WBC casts
4.2.2.2.4. leukocytosis
4.2.2.2.5. cystitis symptoms
4.2.2.3. Etiology
4.2.2.3.1. E Coli (90%)
4.2.2.3.2. Enterococcus Faecalis
4.2.2.3.3. Klebsiella
4.2.3. Chronic Pyelonephritis
4.2.3.1. patho
4.2.3.1.1. multiple abouts of acute pyelophritis
4.2.3.2. etiology
4.2.3.2.1. Kids
4.2.3.2.2. Adults
4.2.3.3. Findings
4.2.3.3.1. Cortical scarring
4.2.3.3.2. blunted calyxes
4.2.3.3.3. scarring at upper and lower poles
4.2.3.3.4. thyroidization
4.2.3.3.5. waxy casts
4.3. by Findings
5. Chronic Renal Failure aka ESKD
5.1. caused by
5.1.1. glomuular probs
5.1.2. tubular probs
5.1.3. inflammatory probs
5.1.4. vascular probs
5.2. Etiologies
5.2.1. DM
5.2.2. HTN
5.2.3. Glomerular disease
5.3. Findings
5.3.1. Uremia/Azotemia
5.3.1.1. nausea
5.3.1.2. anorexia
5.3.1.3. pericarditis
5.3.1.4. plt dysfucntion
5.3.1.5. encephalopathy with asterixis
5.3.1.6. deposition of urea cyrstals in skin
5.3.2. Salt and water retention
5.3.2.1. HTN
5.3.3. Hyper kalemia
5.3.3.1. metabolic acidosis
5.3.3.1.1. icnreased anion gap
5.3.4. decreased EPO
5.3.4.1. anemia
5.3.5. Hypocalcemia
5.3.5.1. decreased 1-a-hydroxylatio of Vit D by PCT
5.3.5.2. Hyperphostatemia
5.3.6. Renal osteodystrophy
5.3.6.1. secondary hyperparathyroidism
5.3.6.2. osteomalacia
5.3.6.2.1. don't have calcium to solidify phosphtte crystalsa nd make bone
5.3.6.3. osteoporiss
5.3.6.3.1. leech from bone b/c metabolic acidosis
5.3.6.4. osteitis fibrosa cystica
5.3.6.4.1. break down bone to make up for Ca
5.4. treatment
5.4.1. dialysis
5.4.2. transplant
5.5. complications
5.5.1. dialsysis
5.5.1.1. cysts
5.5.1.2. shrunken kidneys
5.5.1.3. increasing change of renal cell carcinoma
6. Lower Urinary tract Carcinoma
6.1. Urothelial (Transitional Cell) Carcinoma
6.1.1. arises from
6.1.1.1. urothelial lining of
6.1.1.1.1. renal pelvis
6.1.1.1.2. ureter
6.1.1.1.3. bladder
6.1.1.1.4. urethra
6.1.2. pathophys
6.1.2.1. malignant
6.1.2.2. often mutifocal
6.1.2.3. recur
6.1.2.4. "field defect"
6.1.2.5. most common in bladder
6.1.3. note:
6.1.3.1. most common type of lower urinary tract cancer
6.1.4. risk factor
6.1.4.1. smoking
6.1.4.2. naphthylamine
6.1.4.2.1. in cig smoke
6.1.4.3. azo dyes (hair dyes)
6.1.4.4. long term drug use
6.1.4.4.1. cyclophosphamide
6.1.4.4.2. phenacetic
6.1.5. demo
6.1.5.1. older adults
6.1.6. presentation
6.1.6.1. painless
6.1.6.2. hematuria
6.1.7. Etiology
6.1.7.1. 2 pathways
6.1.7.1.1. Flat
6.1.7.1.2. Papillary
6.2. Squamous Cell Carcinoma
6.2.1. Patho
6.2.1.1. Malignant
6.2.1.2. squamous cells
6.2.1.3. mc with bladder
6.2.1.4. starts with metaplasia to squamous (from transitional)
6.2.1.4.1. then becomes dysplastic
6.2.2. risk factors
6.2.2.1. chronic cystitis
6.2.2.2. Schisto
6.2.2.3. long-standing nephrolithiasis
6.2.3. demo
6.2.3.1. odler woman
6.2.3.2. Egyptian male
6.3. Adenocarcinoma
6.3.1. Patho
6.3.1.1. malignant
6.3.1.2. prolif of glands
6.3.1.3. usually bladder
6.3.2. Etiology
6.3.2.1. from urachal remnant
6.3.2.1.1. develops at dome of bladder
6.3.2.2. cystitis glandularis
6.3.2.2.1. columnar hyperplasia
6.3.2.3. exstrophy
6.3.2.3.1. congenital failure to form the caudal portion of the ant abd and bladder walls
7. Hydronephrosis
7.1. Causes
7.1.1. Obstruction
7.1.2. Compression
7.2. Who
7.2.1. fetus
7.2.1.1. cause unknown
7.2.1.2. often resolves
7.2.2. Third Trimester
7.2.2.1. vesicouretal reflex
7.2.2.1.1. retrograde flow of urine from bladder into urinary tract
7.2.2.2. congenital uretopelvic obstruction
7.2.2.2.1. problem/blockage of urine leaving renal pelvis
7.2.3. young child
7.2.3.1. Congentital malformations
7.2.3.1.1. uretoerocele
7.2.3.1.2. posterior urethral valves
7.2.4. Adults
7.2.4.1. Acquired Disease
7.2.4.1.1. Kidney Stones
7.2.4.1.2. BPH
7.3. Presents with
7.3.1. Obstructive
7.3.1.1. Flank Pain
7.3.1.2. Groin Pain
7.3.1.3. UTI
7.3.2. Hydronephrosis
7.3.2.1. post renal azotemia
7.3.2.1.1. increased N reabsoprtion
7.4. DX:
7.4.1. US
7.4.2. Intrauretal urography
7.4.3. Intrauretal pyelography
7.4.4. CT
7.5. Tx:
7.5.1. relieve obstruction
7.5.1.1. acute
7.5.1.1.1. nephrostomy tube
7.5.1.2. Chronic
7.5.1.2.1. Ureteric stent
7.5.1.2.2. Pyeloplasty
7.5.1.3. Lower obstruction
7.5.1.3.1. Urinary catheter
7.5.1.3.2. Suprapubic catheter
8. Congenital
8.1. Horshoe Kidney
8.1.1. How
8.1.1.1. 1- Mechanical Fusion
8.1.1.1.1. at 5 wks (metanephros)
8.1.1.1.2. flexion pushes kidneys together
8.1.1.1.3. inferior poles touch and fuse
8.1.1.1.4. leads to isthmus
8.1.1.2. 2-Teratogenic event
8.1.1.2.1. Posterior Nephrogenic cells migrate to posterior pole of kidney (wrong spot)
8.1.1.2.2. leads to isthmus
8.1.2. Complications
8.1.2.1. Stuck on Inferior mesenteric artery on ascention
8.1.2.2. leads to lower placement
8.1.2.3. can cause compression of kidney
8.1.2.4. can cause hydropnephrosis
8.1.3. associations
8.1.3.1. Kidney stones
8.1.3.2. Infection
8.1.3.3. Chromosomal Disorders
8.1.3.3.1. Turner
8.1.3.3.2. Trisomies 13,18,21
8.1.3.4. increased risk of
8.1.3.4.1. kidney cancer
8.1.4. Demographics
8.1.4.1. common
8.1.4.1.1. 1:500
8.1.4.2. men>women
8.1.5. Symptoms
8.1.5.1. normally asymptomatic
8.1.6. Tx
8.1.6.1. normally not necessary
8.1.6.2. might need sx if leads to complication
8.2. Obstructive (see Hydronephrosis)
8.2.1. Primary Vesicouretal Reflux
8.2.1.1. Notes
8.2.1.1.1. Most common
8.2.1.2. Pathogenesis
8.2.1.2.1. Primary
8.2.1.2.2. Secondary
8.2.1.3. Grades
8.2.1.3.1. How far urine backs up
8.2.1.4. Dx:
8.2.1.4.1. Abdominal US
8.2.1.4.2. Voiding Cystourethrogram (VCUG)
8.2.1.4.3. Radionuclide Cystogram
8.2.1.5. Treatment
8.2.1.5.1. child
8.2.1.5.2. Severe
8.2.2. Posterior uretrhal valve aka Congenital Obstructive Posterior urethral membrane
8.2.2.1. Demographs
8.2.2.1.1. Boys
8.2.2.2. Pathogenesis
8.2.2.2.1. membranous folds of posterior urethra (closest to bladder) obstruct realeasing of bladder
8.2.2.2.2. disruption in development bt 9-14 wks in utero
8.2.2.3. Complications
8.2.2.3.1. Oligohydramnios
8.2.2.3.2. urine backup
8.2.2.3.3. Increased Bladder pressure
8.2.2.3.4. Chornic Kidney Disease
8.2.2.4. Diagnosis
8.2.2.4.1. US
8.2.2.5. Treatment
8.2.2.5.1. Surgery and Ablation
8.3. Renal Agenesis
8.3.1. types
8.3.1.1. unilateral
8.3.1.1.1. Symptoms
8.3.1.1.2. Complications
8.3.1.2. bilateral
8.3.1.2.1. Problems start in utero (wk 16)
8.3.1.2.2. Prognosis
8.3.2. cause
8.3.2.1. uretic bud fails to induce metanephric blastema
8.3.3. pathogenesis
8.3.3.1. genetic factors
8.3.3.2. environmental factors
8.3.3.2.1. toxins
8.3.3.2.2. infecitons
8.4. Cystic Kidney Diseases
8.4.1. By Symptom
8.4.1.1. Size
8.4.1.1.1. Shrunken
8.4.1.1.2. Hypertrophy
8.4.1.2. Kidneys affected
8.4.1.2.1. Unilateral
8.4.1.2.2. Bilateral
8.4.1.3. Location of Cysts
8.4.1.3.1. Renal Cortex
8.4.1.3.2. Renal Medulla
8.4.1.3.3. Parenchyma
8.4.1.3.4. Corticomedullary jxn
8.4.1.4. Etiology
8.4.1.4.1. Noninherited
8.4.1.4.2. Genetic
8.4.1.5. Age
8.4.1.5.1. Infant
8.4.1.5.2. Child/Adult
8.4.2. By Disease
8.4.2.1. Mulitcystic Dysplastic Kidney (MCKD)
8.4.2.1.1. Cause
8.4.2.1.2. Pathogenesis:
8.4.2.1.3. Presentation
8.4.2.1.4. Associated with
8.4.2.1.5. Treatment
8.4.2.2. Polycystic Kidney Disease
8.4.2.2.1. 2 Types
8.4.2.2.2. Symptoms
8.4.2.2.3. Diagnosis
8.4.2.2.4. Complications
8.4.2.2.5. Treatment
8.4.2.3. Medullary Cystic kidney disease
8.4.2.3.1. Cause
8.4.2.3.2. Pathogenesis
8.4.2.3.3. Demo
8.4.2.3.4. Presentation
8.4.2.3.5. Complications
8.4.2.3.6. Findings
8.4.2.3.7. Dx
8.4.2.3.8. Treatment:
8.4.2.4. Nephronophthisis
8.4.2.4.1. Cause
8.4.2.4.2. Characterized as
8.4.2.4.3. Demographics
8.4.2.4.4. Subtypes
8.4.2.4.5. Pathogenesis
8.4.2.4.6. Presents with
8.4.2.4.7. Associated with
8.4.2.4.8. Complications
8.4.2.4.9. Findings
8.4.2.4.10. Dx
8.4.2.4.11. Treatment:
8.4.2.5. Medullary Sponge Kidney
8.4.2.5.1. aka Cacchi-Ricci Disease
8.4.2.5.2. Cause
8.4.2.5.3. Demo
8.4.2.5.4. Pathogenesis
8.4.2.5.5. Presentation
8.4.2.5.6. Complications
8.4.2.5.7. Dx
8.4.2.5.8. Tx
9. Other Causes
9.1. Amniotic Rupture
9.2. Uteroplacenta Insufficiency
9.2.1. low blood flow to placenta
9.3. Atresia of Ureter or Urethra
10. Nephrolithiasis
10.1. Kidney Stones
10.1.1. Types
10.1.1.1. Calcium
10.1.1.1.1. Caused by/risk factors
10.1.1.1.2. Imaging
10.1.1.1.3. Calcium Oxalate
10.1.1.1.4. Calcium Phosphate
10.1.1.2. Struvite
10.1.1.2.1. aka: Magnesium Ammonium Phosphate Stones
10.1.1.2.2. Caused by
10.1.1.2.3. Shape
10.1.1.2.4. Treatment
10.1.1.2.5. Imaging:
10.1.1.3. Uric Acid
10.1.1.3.1. Caused by
10.1.1.3.2. Associated with
10.1.1.3.3. Shape
10.1.1.3.4. Imaging
10.1.1.3.5. Treatment:
10.1.1.4. Cystein
10.1.1.4.1. Caused by
10.1.1.4.2. Findings
10.1.1.4.3. Shape
10.1.2. Shapes
10.1.2.1. hexagonal
10.1.2.1.1. Cystine
10.1.2.2. envelope
10.1.2.2.1. Calcium oxalate
10.1.2.3. wedge-shaped prism
10.1.2.3.1. Calcium Phosphate
10.1.2.4. Rhomboid or rosettes
10.1.2.4.1. Uric Acid
10.1.2.5. dumbell
10.1.2.5.1. Calcium Oxalate
10.1.2.6. coffin lid
10.1.2.6.1. Struvite
10.1.3. Presents with
10.1.3.1. unilateral flank tenderness
10.1.3.2. colicky pain radiating to goin
10.1.3.3. hematuria
10.1.3.4. Obstruction s
10.1.4. treatment
10.1.4.1. fluid intake
10.1.4.2. plus situation
10.1.4.2.1. Thiazide
10.1.4.2.2. citrate
10.1.4.2.3. urine alkalinization etc
11. Renal Neoplasia
11.1. Angiomyolipoma
11.1.1. Patho
11.1.1.1. Hamartoma
11.1.1.1.1. blood vessels
11.1.1.1.2. smooth muscle
11.1.1.1.3. adipose tissue
11.1.2. Associations
11.1.2.1. Tuberous sclerosis
11.2. Renal Cell Carcinoma
11.2.1. Pathophys
11.2.1.1. Malignant
11.2.1.2. epithelial tumor
11.2.1.3. from kidney tubules
11.2.2. Pathogenesis
11.2.2.1. genetic
11.2.2.1.1. AD
11.2.3. Presentation
11.2.3.1. Triad
11.2.3.1.1. triad doesn't typically occur together
11.2.3.1.2. Hematuria
11.2.3.1.3. palpable mass
11.2.3.1.4. flank pain
11.2.3.2. fever
11.2.3.3. weight loss
11.2.3.4. paraneoplastic syndrome
11.2.3.4.1. increase in
11.2.3.5. Left-sided varicocele
11.2.3.5.1. blockage of drainage of L spermatic cord
11.2.3.6. Sporadic
11.2.3.6.1. Upper pole of kidney
11.2.4. 2 Etiologies
11.2.4.1. Hereditary
11.2.4.1.1. Demo
11.2.4.1.2. Presentaiton
11.2.4.2. Sporadic
11.2.4.2.1. demo:
11.2.4.2.2. presentation:
11.2.4.2.3. risk factor:
11.2.5. Findings
11.2.5.1. gross yello mass
11.2.5.2. microscoppic clear cytoplasm
11.2.6. Staging
11.2.6.1. T
11.2.6.1.1. based on size and involvement of the renal veins
11.2.6.1.2. loves to go to vein
11.2.6.2. N
11.2.6.2.1. spread to retroperitoneal lymph nodes
11.3. Wilm's Tumor
11.3.1. Note:
11.3.1.1. most common malignant renal tumor in children
11.3.2. Demo
11.3.2.1. Children
11.3.2.1.1. avg age =3
11.3.3. Pathophys
11.3.3.1. malignant tumor
11.3.3.2. made of
11.3.3.2.1. Blastema
11.3.3.2.2. primitive glomeruli
11.3.3.2.3. primitive tubules
11.3.3.2.4. stromal cells
11.3.4. presentaiton
11.3.4.1. large flank mass
11.3.4.2. unilateral
11.3.4.3. hematuria
11.3.4.4. HTN
11.3.4.4.1. secondary to renin secretion
11.3.5. Etiology
11.3.5.1. Sporadic 90%
11.3.5.1.1. WAGR syndrome
11.3.5.1.2. Densy-Drash syndrome
11.3.5.1.3. Beckwith-Wiedemann syndrome