Post-Renal Distended bladder on exam. Large volume diuresis after passing urinary catheter. Bilateral hydronephrosis on ultrasound. Post-void residual > 200 ml is suspicious. Black arrow = renal capsule Black arrowhead = sinus fat White arrow = dilated calyx White arrowhead = renal cortex
Hydronephrosis Large hypoechoic area (black on U/S = no echoes) in center of kidney. Dilation extends into the parenchyma. The normal hyperechoic area in the center of the kidney (hilum) is replaced by a large hydronephrotic renal pelvis. This kidney has hydronephrosis due to obstruction of upper ureter.
Treatment of Obstruction Lower tract: Foley cath. Upper tract: Ureteral stent or percutaneous nephrostomy.
Pre-renal Hypotension. Hypovolemia (decreased renal perfusion). CHF: pump doesn’t work, can’t perfuse kidney. Constrictive pericarditis: heart cannot fill, can’t perfuse kidney. GI Bleed (digested blood is source of urea). Excess diuresis. Dehydrated patient may have high BUN (azotemia) due to lack of fluid volume to excrete waste products. Nothing wrong with kidney itself – will try to absorb sodium to maintain volume. Treat the underlying cause! Pre- renal usually improves with IVF
Intra-Renal Acute Tubular Necrosis (ATN) Caused by hypoperfusion to the point of tubular cell death or from toxic injuries. Muddy Brown Casts
ATN (continued) Typically begins immediately after study. Renal function recovers after 3-5 days. Prevent: Hydration, ½ NS 75 cc/hr 8-12 hr before and after study. Acetylcysteine 600 mg BID for 2 days if diabetes, CHF, CRI. Begins at least 5 days after treatment. Contrast NephropathyAminoglycoside Toxicity
Rhabdomyolysis leading to ARF Labs: CPK elevated, Urine dipstick (urinalysis best initial test) shows blood but no RBC on microscopy. Urine myoglobin most accurate. Tx: IVF, IV sodium bicarbonate to alkalinize urine to solubilize myoglobin. Mannitol and diuresis decrease contact time of myoglobin with tubule.
Clinical Situation Patient is brought to the emergency room after a seizure leading to prolonged immobility on sidewalk. Next step? A) Urinalysis B) Urine Myoglobin C) EKG D) CPK E) Phosphate level F) Creatinine
Acute Rhabdomyolysis EKG most urgent step. Severe muscle necrosis leads to Hyperkalemia. Look for peaked T waves. Treat with immediate IV calcium gluconate, insulin, glucose. Order Potassium level (cellular destruction). Order Calcium level (hypocalcemia): damaged muscle may bind increased calcium. Hyperphosphatemia may lead to calcium binding with phosphate. Order chemistries to detect decreased serum bicarb.
IgA Nephropathy (Berger’s Disease) History of URI 1-2 days before presentation + Painless recurrent hematuria Recurrent hematuria following exertion Serum IgA increased in 50% of patients Normal complement Renal Biopsy to confirm Treatment: ACE inhibitor and ARB Consider adding Fish Oil Prednisone if tx-refractory or nephrotic syndrome/markedly proliferative disease.
IgA Nephropathy Biopsy: Mesangial Hypercellularity
IgA Nephropathy Immunofluorescence IgA mesangial deposits = characteristic and defining feature of the disease Deposits are exclusive of IgA in only ~26% of cases; usually accompanied by IgG (~37%) or IgM (~13%), and the three Igs may be present in ~25% of cases. However, IgA must be dominant or codominant
Post-streptococcal GN URI 7-10 days before presentation “Cola or tea” colored urine Periorbital edema/HTN ASO titer, Low serum complement Treat infection/HTN
Clinical Scenario Patient with sinusitis, rhinorrhea, bloody nasal discharge and cough, shortness of breath, hemoptysis. Hematuria, Proteinuria and Renal Failure. + for c-ANCA Most likely diagnosis?
Wegener’s granulomatosis Confirm with biopsy of nasopharyngeal lesion if possible. Alternative: renal biopsy (crescentic necrotizing GN). Focal or diffuse necrotizing extracapillary GN is histological hallmark of ANCA-associated Vasculitis. Tx: Corticosteroid and Cyclophosphamide
Electron Microscopy Normal vs. MCD Normal Kidney MCD: The individual foot processes can no longer be made out- they have all just “melted” together into a single thin layer. Barrier in filtration process can no longer keep protein from being filtered out of the blood and into urine.
Membranous Nephropathy Most common cause of Nephrotic syndrome in adults. Causes: idiopathic, carcinoma, Hep B, Hep C, SLE, Drugs: Penicillamine, Captopril, Gold Treatment: Prednisone
Kidney Biopsy Review When all or at least more than 80% of the glomeruli seen in the biopsy is affected. Only certain proportion of the glomeruli seen in the biopsy involved. DIFFUSEFOCAL
Kidney Biopsy Review When the entire globe of the glomerulus is affected. Only a segment of glomerulus involved. GLOBALSEGMENTAL
Focal Segmental Glomerular Sclerosis Most common cause of Nephrotic syndrome in black patients, obese patients, IVDA, heroin abuse, HIV.
Normal pH 7.4 = 40 nmol/L 24 X 40/24 H + = 24 X PCO2 (respiratory)/HCO3- (metabolic) pH < 7.4 is acidotic
Normal anion gap (8-12 mEq/L) Diarrhea Glue sniffing Renal tubular acidosis Hyperchloremia
Metabolic Acidosis: Compensation For every 1 mEq HCO3- down, there is 1.3 mmHg PCO2 down Increased ventilation, blow off CO2
Metabolic Alkalosis Vomiting (urine chloride < 20) Diuretic use (except carbonic anhydrase inhibitors): Ucl>20 Antacids/milk-alkali syndrome Hyperaldosteronism Bicarbonate addition Loss of H+ from GI tract or kidney Loss of Chloride from GI tract or kidney Adaptation: 0.7 mm Hg of PCO2 up for every 1mEq/L up of HCO3- Decrease ventilation!
Respiratory Acidosis Primary disturbance? PCO2 Up Acute causes: Airway obstruction Status asthmaticus Alveolar defects (pulmonary edema, pneumonia) CNS depression, neuromuscular impairment Ventilatory restriction (flail chest with rib fractures) Chronic causes: COPD, abnormal chest wall mechanics. Compensation: Acute (for any PCO2 up go 1-3 mEq/L up in HCO3-) Chronic: For any 1 mm Hg up in PCO2 go up 0.4 mEq/L in HCO3-)
Clinical Scenario: Aspirin Overdose Causes two different primary disturbances: Respiratory Alkalosis and Metabolic Acidosis Look for co-existing tinnitus, hypoglycemia, vomiting, history of “swallowing several pills.” Alkalinize urine with Bicarbonate: speeds excretion.
Diabetes insipidus Lab: Urine osmolality less than serum. How do you differentiate between central and nephrogenic DI? Vasopressin challenge: Uosm increases in central, minimal change in nephrogenic.
Central vs. Nephrogenic DI Central: Decreased production of vasopressin (trauma, neurosurgery, idiopathic). Treatment: intranasal DDAVP. Nephrogenic: renal tubules unresponsive to vasopressin (Lithium, Demeclocycline, hypokalemia, hypercalcemia). Treat the cause, thiazide or amiloride.
Clinical Scenario 78 year old male from nursing home with altered mental status, serum sodium 160. BUN/Cr high and Uosm very high >800. Started DSW: after 10 hours the patient developed a seizure. What happened? Rapid correction of hypernatremia. In hypernatremic patient: slow correction 0.5 mEq/L per hour by free water or D5W (no more than 12 mEq/L over first 24 hours). Check serum sodium every 2 hours!
Hyponatremia In True hyponatremia: Serum Osmolality should be low. Hyponatremia with normal plasma osmolality: Pseudohyponatremia due to hyperlipidemia or hyperproteinemia. Hyponatremia with elevated plasma osmolality: mannitol or hyperglycemia. For every 100 above 100 mg/dl of glucose > correct serum Na Example: Plasma glucose 400 and Serum Na+ 130 > corrected will be 134.8
Treatment of Hyponatremia Asymptomatic: increase serum sodium 0.5 mEq/L per hour (10-12 mEq/L per day). Hypovolemia: Use Normal saline. Hypervolemia, SIADH: FLUID RESTRICTION! Symptomatic: Hypertonic saline, 1-2 mEq/L per hour first 3-4 hr then mEq/L per hour. No more than mEq/L per day in first 24 hours.
Rapid Correction of Hyponatremia Central Pontine Myelinolysis or Osmotic Demyelination Syndrome (flaccid paralysis, dysarthria, dysphagia).