Nephrology for Studs

NEPHROLOGY

 Pre-renal Azotemia - ↑ BUN but creatinine near normal (N) (0.6 – 1.2)
 Post-renal Azotemia - ↑ BUN & ↑ creatinine
 Renal Azotemia – BUN/Cr ≤ 15 ( bcoz more ↑↑ in creatinine)
 Cortical necrosis of both kidney sparing medulla – DIC
 Sickle cell anemia – affect medulla most severly – can cause Papillary necrosis
 Renal papillary necrosis (SADD) – Sickle cell anemia, Acute pyelonephritis,
Drugs (Aspirin + acetaminophen), Diabetes
* Nephritic type Glomerular Disease : (moderate proteinuria & RBC cast)
 IgA glomerulonephritis (Berger’s disease) (Buerger’s disease –
thromboangitis obliterans – male – smoking cigarettes) (both are different
disease) – episodic bouts of hematuria 1-3 days following URTI, slow
progression to CRF (40-50%), mesangeal IgA deposit with granular
immunoflurocence
 Post-streptococcal – Hematuria 1-3 weeks following group A Strep Pyogens
infection
- Skin infection - ↑ anti-DNAase B titer
- Pharynx infection - ↑ ASO titer
- Diffuse proliferative (usually resolve, CRF is uncommon)
 Diffuse Proliferative (SLE) – subendothelial Immune Complex (IC) (anti-ds
DNA Ab) deposit with granular IF, “wire looping” of capillaries (CRF most
common cause of death in SLE)
 Rapidly Progressive – crescent formation, associated with Goodpasture
syndrome (linear IF) (Lower Resp Tract involvement, Hemoptysis followed
by ARF), Polyarteritis nodosa (p-ANCA) (GIT involvement – mesenteric
artery, bowel ischemia, bloody diarrhea), Wegner’s granulomatosis (c-
ANCA) (Upper & Lower Resp Tract involvement, perforation of nasal
septum)
* Nephrotic type Glomerular Disease : (proteinuria› 3.5 g/24 hrs & fatty cast)
 Minimal change disease – children – EM show fusion of podocytes
(selective proteinuria – Albumin not globulin), negative IF
 Focal Segmental – HIV, Heroin IV abuse, NSAID, Hodgkin’s lymphoma –
negative IF, non-selective proteinuria
 Diffuse Membranous – Adults – captopril, HBV, malaria, syphilis –
subepithelial deposit with granular IF – “spike and dome” pattern
 Type-1 MPGN – HCV, HBV, cryoglobulinemia – subepithelial deposit – EM
show “tram track” (progress to CRF)
 Type-2 MPGN – C3 nephritic factor (C3NeF), Ab binds to C3 convertase &
prevent its degradation & sustain activation of C3 leads to very low C3 level.
“dense deposit disease” (progress to CRF)

 Only in SLE, there is subendothelial deposit. In all others, there is subepithelial
deposit
 Only in Goodpasture syndrome, there is linear deposit. In all others, there is
granular deposit.
 Patient with Nephrotic syndrome has accelerated athrogenesis
 Palpable purpura, hematuria, Proteinuria, Hepatitis C – diagnosis?  Mixed
essential cryoglobulinemia – Tx: Mix cryoglobulinemia associated with Hep C –
Anti-viral drugs (Ribavirin and alpha-interferon)
 Polyarteritis nodosa – p-ANCA – HbsAg (+) in 30% of cases
 Lichen planus – association with Hep. C
 Glomerular nodule – DM / Amyloid (chronic disease) both show red on H&E
stain but with Congo red stain – Amyloid – “apple-green” birefringence nodule.
DM nodule is composed of Type-4 collagen & protein
 Pathogenesis of DM: Nonenzymatic glycosylation (glucose + AA) → ↑vessel
permeability to protein and ↑athrogenesis; Osmotic damage → Aldolase
reductase (glucose → sorbitol) → sorbitol draws water into tissues causing damage
(eg. retinopathy); Diabetic microangiopathy → ↑synthesis of type-IV collagen in
basement membrane & mesangium
˗ Tight blood sugar control decrease the risk of development of microvascular
complication (retinopathy, nephropathy, neuropathy)
˗ ACE inhibitors has shown to reduce insulin resistance
 Screening test for nephropathy in DM: Random urine for microalbumin /
creatinine ratio
 Earliest renal abnormality seen in diabetic nephropathy: glomerular hyper
filtration
 Ethylene glycol poisoning – Metabolic acidosis (↑ anion gap) + oxalate
crystalluria
 Cystinuria – staghorn calculi, positive nitropruside cyanide test
 Staghorn calculi – Proteus infection
* Acid-Base Disturbances
 (Na + K) – (HCO3 + Cl) = 8-14 (normal anion gap)
 Only chronic acidosis/alkalosis is compensated not acute
 Chronic Resp. Acidosis – compensated by Metabolic Alkalosis (HCO3 – 22-28)
PCo2 - › 45 mmHg, HCO3 - ≤ 30 mEq/L – Acute Resp. Acidosis
HCO3 - › 30 mEq/L – Chronic Resp. Acidosis
 Chronic Resp. Alkalosis – compensated by Metabolic Acidosis
PCo2 - ‹ 33 mmHg, HCO3 - ≥ 18 mEq/L – Acute Resp. Alkalosis
HCO3 - ‹ 18 mEq/L (but›12 mEq/L) – Chronic Resp. Alkalosis

* Renal Tubular Acidosis (Normal Anion gap Acidosis)
 Type-1 – secondary to autoimmune diseases, Lithium, analgesics, sickle cell
disease
Inability to secrete H+ in Urine, Urine pH - › 5.4
Patient usually gets Renal stone
Acid load Test – After giving ammonium chloride, urine pH still remain elevated
(normally it should be decreased)
 Type-2 – Renal threshold for absorbing HCO3 is lowered from normal of 24
mEq/L to 15 mEq/L
Initially pH › 5.5 and then it goes back to ‹5.5
Patient usually get bone lesion (osteomalacia, rickets)
Both Type-1 & Type-2 get Hypokalamia.
 Type-4 is the only renal tubular acidosis which produce hyperkalamia due to
destruction of JG apparatus - ↓ rennin - ↓ aldosterone
Causes – hyaline arteriosclerosis in afferent arteriole in DM, Legionaire’s disease
 Intake of salt = output of salt (95% renal & 5% sweat)
* Hyponatremia – Na ‹135 in the absence of hyperglycemia
 SIADH – Oral hypoglycemic & Carbamazapine
 Diagnosis – Urine osm › Serum osm (Urine osm › 40 is typical)
 Treatment – fluid restriction (hyponatremia due to volume overload like in CHF),
loop diuretics & normal saline, hypertonic saline, Lithium/Demeclocycline in
SIADH. Rapid correction of hyponatremia results in Central Pontine Myelinosis
– destruction of brain stem present with paraparesis, dysarthria or Dysphagia.
* Hypernatremia – loss of hypotonic fluids (sweating, burns, fever), central DI &
Nephrogenic DI – Best initial Tx of hypovolemic hypernatremia – normal saline
(0.9%)
* Hypokalamia – “U” wave on ECG, Alkalosis, ↑ Aldosterone
* Hyperkalemia – peaked T wave on ECG, Acidosis, ↓ Aldosterone – IV calcium
gluconate (first step) – In Hyperkalemia, removal of k+ from the body can be
achieved by dialysis, cations exchange resins (kayexalate) or diuretics.
* Hypercalcemia – IV normal saline infusion (first step). (except hypercalcemia is
due to Metastasis in which bisphosphonates preferred)
* Hypophosphatemia – continuous infusion of glucose is the leading cause of
hypophosphatemia; muscles weakness
* Hypercalcemia – Loop diuretics / Hypercalciuria – Thiazide diuretics
· Any time in question, hypokalamia, first step – IV potassium
· Any time in question, hyperkalemia, first step – IV calcium gluconate
· Hypocalcemia – hyperactive deep tendon reflexes
· Hypermagnesemia – loss of deep tendon reflexes

* Pheochromocytoma
 a neuroendocrine tumor of the medulla of the adrenal glands
 Signs & Symptoms of sympathetic hyperactivity (increase HR, HTN, etc)
 Diagnosis : urinary vanillylmandelic acid (VMA)
 CT scan/MRI – to localize tumor
 Confirmation of diagnosis with biochemical tests (24-hrs urine measurement of
VMA, metanephrines & catecholamine) is required before imaging studies. Once
diagnosis is confirmed, start alpha-blockers.
 Treatment – Alfa-blockade followed by surgical removal
* Renal Artery Stenosis
˗ Best screening test – US abdomen (renal Doppler US) / captopril renogram (best
non-invasive method)
˗ Most accurate method – MRI / CT angiography
˗ Best initial treatment – percutneous transluminal angioplasty
* MCC of secondary HTN in children – fibromuscular dysplasia (20% of all cases
of renal HTN) – angiogram typically show a “string of bead” appearance to the
renal artery
* Important Urinary Cast
 Waxy, broad cast – signs of End Stage Renal Disease
 WBC cast – Acute pyelonephritis, acute tubulointerstitial nephritis (drug)
 Renal tubular cell cast (muddy brown granular cast) - ATN
· First step in management of patient with hematuria – urine analysis
· Microscopic / gross painless hematuria, next step? – CT urogram / IVP (to look
kidney & ureter) and Cystoscopy (to look bladder)
· Most common cause of painless hematuria in adults in USA  Bladder mass then
Renal cell CA
· Patient with BPH doesn’t have hematuria. Presence of hematuria in a patient with
BPH present with irritative or obstructive voiding symptoms – always suspect
bladder CA
· Chronic pyelonephritis: h/o vasicoureteral reflux + bilateral focal parenchymal
scaring & blunted Calyces on IVP
 Chronic Renal Failure (CRF) :
· Diabetic nephropathy, HTN and glomerulonephritis [These 3 = 75% of cases]
· Volume overload leads to HTN and CHF
· Uremia (Pericarditis and encephalopathy)
· Hyperkalemia, Hyperphosphotemia and Hypocalcemia (Vit-D3 deficiency) (renal
osteodystrophy)
· Metabolic acidosis and accelerated atherosclerosis
· Causes of bleeding in CRF – platelet dysfunction

· Increase Bleeding Time due to renal disease – IV Desmopressin (first choice)
· CRF patient should receive erythropoietin & iron supplementation
· Anemia in patient with end-stage renal disease is due to erythropoietin deficiency.
If there is no or minimal increase in hematocrit level after 4-6 wks treatment with
EPO, iron saturation, ferritin level and TIBC should be measure [Side effects of
Erythropoietin Therapy – worsening of hypertension, Headache, flu-like
syndrome, Red cell aplasia]
· Vitamin-D3 and calcium supplements, ACE inhibitors have been found to slow
the progression of CRF
· Protein restriction improve prognosis in CRF
 Kidney stones – plain X-ray KUB (first step); If KUB is normal but S&S
suggestive of renal stone, next step? – order CT scan without contrast; Pregnant
patient with S&S of renal stone, next step? – order U/S of abdomen
 Urethral Diverticulum – h/o frequent UTI, tender suburethral mass – classical
triad of dribbling, dyspareunia and Dysuria – order Cystourethrogram or
Urethroscopy
* Juvenile Polycystic Kidney Disease
 Autosomal recessive
 Bilateral enlarged kidney at birth
 Maternal oligohydramnios
* Adult Polycystic Kidney Disease
 Autosomal dominant
 Bilateral enlarged kidney around 20-25 yrs of age
 Cyst also present in liver (40%)
 Intracranial berry aneurysm (10-30%) (present with subarachnoid hemorrhage),
HTN, sigmoid diverticulosis (Before doing peritoneal dialysis in a patient with
APKD, patient should undergo colonoscopy first), MVP
 Follow up plan for patient with APKD – regular BP measurement
 Screening test for APKD – U/S
* Multiple contrast filled cyst on IVP, diagnosis?  Medullary Cystic kidney
(Autosomal dominant, No Hypertension)
* Unilateral flank mass in child > 3 yrs  Wilm’s tumor
Bilateral flank mass in child  polycystic kidney (infantile)
Unilateral flank mass in Adults  Renal cell CA
Bilateral flank mass in Adults  polycystic kidney (adult)
* Renal cell CA (clear cell CA, hypernephroma, Grawitz tumor)
 Derived from proximal tubule (PT)
 Risk factors – smoking, Von Hipple-Lindau syndrome, Adult polycystic kidney
disease (APKD)

 Hematuria, flank mass & CVA tenderness
 Metastasize to lung [cannonball appearance on x-ray], Lt sided varicocele
* Wilms Tumor :
- Derived from mesonephric mesoderm (unilateral flank mass)
- Histology: abortive glomeruli, & tubules, primitive blastemal cells,
rhabdomyoblasts
- Hypertension in child, Autosomal Dominant (chromosome-11)
- WAGR Syndrome (Wilms tumor, Aniridia, Genital abnormalities, Retardation)
* Neuroblastoma :
- N-myc gene amplification.
- Small blue cell tumors (Ewing sarcoma, Lymphoma, Neuroblastoma, small cell
CA of Lung).
- Composed of malignant neuroblast, presence of Homer-Wright rosettes.
- Neurosecretory granules on electron microscopy .
- Hypertension in child.
- Urinary VMA (vanillylmandelic acid), HVA, metanephrines.
 Potter’s syndrome – absent of both kidney – oligohydroamnios – failure of
ureteric buds to develop
· Alport syndrome :
- X-linked dominant disorder
- Asymptomatic hematuria , Sensorineural hearing loss
- Renal biopsy : Glomerular Sclerosis , thickened basement membrane tubular
atrophy fibrosis and foam cells.
· Hemolytic Uremic Syndrome ( HUS ) :
- E.Coli (0157 : HS) ® produce Vero toxin ® endothelial cell injury
- Endothelial injury of the kidney results in localized clotting ® RBCs and intrarenal
platelate damage causes microangiopathic anemia and thrombocytopenia
- Approximately 1 week after E.Coli ( 0157 : H7 ) infection , patient develop
oliguria, sign & symptoms of anemia
- ¯ Hb level m drop in platelate count, Hematuria , proteinuria , Helmet cells on
peripheral smear
- D/D : TTP which involves CNS whereas HUS involves kidney.
· Henoch–Schonlein Purpura :
- IgA – mediated vasculitis of small vessels
- Non-thrombocytopenic purpura in children
- Usually follows an URI.
- Tetrad of Abd. Pain, Rash, Renal involvement & Thrombocytopenia.
- Palpable purpuric rash on buttocks
- Intussusception is more common in patient with HSP
- Tx : Corticosteroids

· Combination of obstruction & Infection of Urinary tract : Patient who is
being allowed to pass a ureteral stone spontaneously & who suddenly develop
chills , fever & flank pain. It is a medical emergency due to high chances of sepsis
so order CT scan without contrast to establish diagnosis after starting IV
antibiotics and hydration
˗ Tx : IV antibiotics & immediate decompression of the urinary tract above the
obstruction by either percutaneous nephrostomy or ureteral stent placement
■ Post- op – Zero urinary output ® plugged / kinked catheter.
■ Post – op – Low urinary output with good perfusing pressure (SBP› 90 mm Hg)
¯
¯ ¯
Insufficient Fluid intake Acute Renal Failure
¯ ¯
Fluid challenge Test ® 500 ml of RL/NS IV in 10-20 mins
¯ ¯
urinary output no change in urinary output
¯ ¯
Na + concentration ® <> 40 mEq /L

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