Transcript Renal Disease / Eckel Service Overview

Prashanth Thakker
 Understand how to accurately diagnose, manage, and treat
acute kidney injury
 Understand the etiology of chronic kidney disease and
management of risk factors to reduce progression
 Manage patients with end stage renal disease by learning
about indications for dialysis and common complications in
the patient population
 Hypertension and electrolytes will be discussed at a later
date**
Get a good history (Baseline)
Stop offending agents
Treat underlying etiology
 An acute/abrupt worsening of renal function (<48
hours)
 ↑ Cr > 0.3mg/dl
 ↑ Cr >50% from baseline
 UOP <0.5mL/kg/hr for >6 hours
 History, history and more history
 Evaluate the urine for sediment
 FeNa or FeUrea
 (Urine Sodium x Plasma Cr)/(Plasma Sodium x Urine Cr)
 (Urine urea x Plasma Cr)/(Plasma Urea x Urine Cr)
 Renal Ultrasound
 Serologies
 Renal Biopsy
 History is key (volume, hemorrhage, ACE-I/ARB/NSAID,
decreased effective circulatory volume – HF, cirrhosis)
 BUN/Cr ratio of >20
 Urine Osm > 500 osm/kg
 FeNa <1%, FeUrea <35%
 Stop agents which could worsen underling azotemia (will
discuss exogenous agents)
 Improve hemodynamics – if renal function improves then
diagnostic and therapeutic
 Systemic Hypotension and…
 Usually associated with prior limited reserve or a co-
existing insult (sepsis, drugs etc.)  tubular and
microvascular changes leading to tubular damage
 More than just hemodynamically mediated…
 Vascular changes in the setting of hemodynamic shift
 Sepsis/Cytokine induced direct endothelial damage
leading to microvascular thrombosis, ROS production etc.
 renal tubular injury
 Rhabdomyolysis  ATN
 History – traumatic crush injury, seizures, prolonged immobility
 Lab findings – elevated myoglobin, CK, UA heme+, low RBC
 Pathophysiology – renal vasoconstriction, direct tubular injury, and
tubular obstr.
 Treatment – fluids
*Hemolysis has a similar mechanism of action
 TLS (Tumor Lysis Syndrome), Multiple myeloma
 In TLS you have precipitation of Uric Acid causing tubular injury
 Severe hypercalcemia can cause significant vasoconstriction and
tubular damage
 Myeloma proteins will precipitate and cause tubular obstruction
 Antimicrobials
 Tubular necrosis – amphotericin B, aminoglycosides
 AIN – PCN, cephalosporins, quinolones, sulfa, rifampin
 Vancomycin w/ high troughs?
 Tubular obstruction – acyclovir
 Direct tubular damage – foscarnet, pentamidine, cidofivir
 Contrast Induced Nephropathy  ATN
 Serum creatinine rises in the first 24-48 hours, with peak 3-5 days
and resolves in 1 week
 Be weary with patient with underling renal disease!!
 Pathophysiology involves direct tubular injury, hypoxia to the outer
medulla due to occlusion of small vessels, transient tube
obstruction
 Fluids (pre-post), +/- bicarbonate
 AIN
 Legionella
 Tubulointerstitial nephritis uveitis (TINU) syndrome
 Acute Nephritic Syndromes (to be discussed)
 TTP/HUS
 Recent GI disease, use of recent calcineurin inhibitors
 Atheroembolic
 Recent vascular manipulation (usually large vessels)
 Stop offending agents and treat underlying condition!!
 Rhabdomyolysis – fluids
 TLS – Allopurinol, Rasburicase
 Volume overload – salt/water restriction, diurese, ultrafiltration
 Hyperkalemia – decrease exogenous K+/meds ↑ K+, transient shift, and Kayexelate
 Metabolic Acidosis – Bicarb if pH <7.2
 Hyperphosphatemia – phosphate binders, phosphate restriction
 DRUG DOSING
 Classification of CKD
 1 (GFR > 90) – Treat underlying condition/comorbidities
 2 (GFR 60 – 89) – Estimate Progression of disease
 3a (GFR 45-59) – Evaluate + treat complications
 3b (GFR 30-44) – Evaluate + treat complications
 4 (GFR 15-29) – Prepare for RRT
 5 (GFR <15) – HD if indicated
 Diabetic Glomerular Disease
 Glomerulonephritis
 Hypertensive Nephropathy
 Primary glomerulopathy with HTN (FSGS)
 Vascular and ischemic renal disease
 ADPKD
 Other cystic and tubulointerstitial kidney disease
1. Diabetic Nephropathy (55%)
2. Hypertensive nephropathy v Hypertension due to
underlying vascular disease (33%)
3. Glomerulonephritis
4. Polycystic Kidney Disease
5. Obstructive Uropathy
 Incidence – 40% patients with DM develop diabetic nephropathy
 Progression usually seen in 5-10 years after DMI (seen as
microalbuminuria), 30-300mg/g of albumin/creatinine ratio is
considered microalbuminuria
 Pathophysiology – increased glomerular pressures, glycosylation
end products cause vascular disruption, filter barrier disruption, and
glomerulosclerosis
 Management – avoid progression through DM II control, blood
pressure control (ACE-I/ARB to reduce intra-glomerular pressure)
 Uncontrolled HTN can cause permanent damage in 6% of patients
with uncontrolled HTN
 Hypertension is the etiology for 27% of patients with ESRD
 Malignant hypertension in the setting of scleroderma and cocaine
use can complicate the progression of hypertensive nephropathy
 ACE-I and adequate blood pressure control is the way to go!
 Nephritic v Nephrotic
 Nephritic
 Blood >> Protein
 1-2g/day, pyuria, hematuria w/ casts, HTN, fluid retention
 Nephrotic
 Protein >> Blood
 3.5g/day (definition) for ‘nephrotic range’ proteinuria
 Nephrotic syndrome
 ANCA + Vasculitis (Pauci-immune) – (40-45%)
 Wegener’s, Microscopic Polyangitis, Churg-Strauss
 Immune Complex Disease (granular) – (40-45%)
 Post strep GN, MPGN, Fibrillary GN, IgA nephropathy
 SLE, Cryoglobinemia, Endocarditis, HSP
 Anti-GBM (linear) - (15%)
 FSGS (40%)
 Idiopathic, HIV, heroin, obesity
 Membranous GN (30%)
 Idiopathic, HBV, HCV
 Minimal Change Disease (20%)
 Idiopathic, NSAIDS
 Membranoproliferative GN (5%)
 Infection (HCV, HBV), immune complex
 Diabetic Nephropathy
 AL/AA Amyloid
 Light-chain deposition disease
 Lupus (WHO class V)
 ADPKD occurs in 1:400–1:1000 individuals worldwide and accounts
for ~4% of end-stage renal disease (ESRD) in the United States via
the ADPKD-1 gene (85%)/ADPKD-2 gene
 Hypertension precedes renal dysfunction
 Associated complications include hepatic cysts, aortic root/annulus
dilation, MVP, AI, Cerebral aneurysms
 Treatment – HTN management, cyst/Pyelo should be treated with
TMP/SMX or fluoroquinolones due to good cyst penetration
 Potassium Hemostasis
 Metabolic Acidosis
 Disorders of Calcium and Phosphate
 Ischemic Vascular Disease
 Heart failure, HTN, LVH
 Anemia
 Abnormal Hemostasis
 Calcium x Phos product
 Calcium containing v non-calcium containing phos binders
 Calcitriol
 Osteitis fibrosa cystica
 Usually starts off as livedo reticularis and then advances to patches of
ischemic necrosis
 Thought to be due to calcification of small-mid sized vessels
leading to ischemia and necrosis
 Associated with high Ca-Phos product > 55
 Management includes local wound care, decrease Ca-Phos product
 Reduction in erythropoietin leads to anemia usually in
stage III or stage IV CKD
 Managed by administration of erythropoietin in
conjunction with iron, vitamin B 12, and folate to ensure
adequate production by the marrow
Progression of CKD or AKI leading to any of the following:
A – ACIDEMIA
E – ELECTROLYTES (↑ K…↑P, ↑Mg, ↓Ca, ↓Na)
I – INGESTION/TOXINS
O – OVERLOAD (UF)
U – UREMIA (pericarditis/encephalopathy)
 Continuous Renal Replacement Therapy
 Intermittent Hemodialysis
 Continuous Ambulatory Peritoneal Dialysis
 Continuous Cyclic Peritoneal Dialysis
 Hypotension
 Muscle Cramps
 Anaphylactoid Reaction to Dialysate
 Type A (IgE-mediated intermediate hypersensitivity reaction) may need steroids
and epi
 Type B non-specific chest and back pain resolve over time
 Continuous Ambulatory Peritoneal Dialysis
 Dialysis solution is manually infused into the peritoneal cavity and exchanged 3-5 times a
day. Gravity is used to move fluid out of the abdomen
 Continuous Cyclic Peritoneal Dialysis
 Dialysis solution is automatically cycled while the patient sleeps
 Complications
 Peritonitis (WBC >100/mm3)
 Non-peritonitis infections
 Weight gain
 Hypoprotenimia
 Etiology of ESRD
 Route of dialysis (HD or PD) – mostly HD
 Location and days of HD (last day of HD)
 Access
 Nephrologist
 Dry Weight
 Review labs closely
 Review medications and make sure renally dosed
 Fever
 Missed Hemodialysis
 Dyspnea
 Hyperkalemia
 Vascular Access
 Chest Pain
 Usually due to line infection, check all access sites! (other etiologies include HCAP,
skin infection, C. dif)
 Cultures peripheral + HD line
 Review prior cultures including MIC (to see if they are building resistance)
 Empiric Treatment
 Cover gram positives for line infection. Gram negatives are covered if there patient is
noted to be fairly ill.
 Vancomycin 20mg/kg load, followed by 10mg/kg post HD
 Zosyn 2,25q8h (HCAP), 2.25q12 otherwise
 Gentamicin is also an excellent choice given with HD
 Volume overload
 Coordinate ultrafiltration with HD unit
 Make sure patient has access, if no access and HD stable can wait for IR to place a line OR
if there is concern for respiratory instability patient should go to MICU for temporary HD
line placement (at this time it would be coordinated with renal MICU fellow)
 Hyperkalemia
 Temporary measures include insulin/D50, Sodium Bicarbonate, Albuterol. You can
stabilize the cardiac membrane with calcium gluconate or chloride. Potassium binding
agent in the GI tract kayexalate can be used
 Keep you senior and renal fellow informed as patient may need HD sooner than you think!
 Important to get history regarding last proper use. It is also
important to examine the patient to look for thrill/bruit any signs of
functionality of the graft or fistula
 Contact Vascular Surgery if there is any concern for thrombosis and
need for declottication
 Again, urgent HD will always require the MICU
 Mr. G is a 65 year old male with a past medical history of CHF presenting with
worsening dyspnea on exertion and orthopnea. Patient notes a 30lb weight gain
over the last month and significant lower extremity edema. He takes Lasix,
Metoprolol Succinate, Lisinopril, Aspirin, and Spironolactone. Patient is afebrile,
blood pressure of 140/90, heart rate 105. Patient is warm and wet with an elevated
JVP and significant +3 lower extremity edema. His labs are consistent with a
creatinine of 2.9 with a baseline of 1.2.
 What do you want to do you think the etiology of the renal dysfunction is in this
patient and what would your plan be?
 Kasper DL, Harrison TR. Disorders of the Kidney and Urinary Tract. In: Harrison's
Principles of Internal Medicine. New York: McGraw-Hill, Medical Pub. Division; 2005.
 Armitage KB et al. Case Approach: A Resident Guide to Internal Medicine at UH Case
Medical Center and the Cleveland VA 2016-2016. Cleveland: Case Medical Center;
2015.
 Sabatine MS. Renal Failure. In: Pocket Medicine. Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkins; 2011.