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CPC July 8 th, 2013 A 65 y/o female with uncontrolled hypertension and acute kidney injury Melanie Braganza, MD, MPH Holly Rosencranz, MD.

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Presentation on theme: "CPC July 8 th, 2013 A 65 y/o female with uncontrolled hypertension and acute kidney injury Melanie Braganza, MD, MPH Holly Rosencranz, MD."— Presentation transcript:

1 CPC July 8 th, 2013 A 65 y/o female with uncontrolled hypertension and acute kidney injury Melanie Braganza, MD, MPH Holly Rosencranz, MD

2 H&P 65 Y/O F Worsening shortness of breath with orthopnea and paroxysmal nocturnal dyspnea for 1 week Non-specific fatigue for several weeks Nausea and vomiting Decreasing urine output Severe neck pain with tingling and numbness in 2 nd and 3 rd fingers of right hand

3 Past Medical History Breast cancer, ER/PR positive stage 4 with metastatic disease to cervical spine, received radiotherapy and was on anastrazole Aug 2012 Recent addition of Fulvestrant for newly noted cervical spine disease Recurrent pleural effusions, non-malignant Pericardial effusion with tamponade s/p emergent pericardiocentesis in Nov 2012 HTN

4 Past surgical history Appendectomy Hysterectomy Pacemaker placement

5 Home medications Benazepril Furosemide Potassium chloride Carvedilol Anastrozole (Arimidex) Fulvestrant (Faslodex)

6 Physical examination Vitals: BP: 239/124 mmHg, HR: 114/min, O2: 99% - 100% on 2 L nasal cannula, T 36.6 C/ 97.9 F General: alert ENT: unremarkable, no icterus Resp: crackles to middle of chest bilaterally, wheezes in upper lobes CV: JVP to jaw, no murmur, RRR, S3, 2 +pitting edema Abdomen: no organomegaly Neurological: alert/oriented, normal strength, tone, reflexes and coordination Skin: no petechiae, no bruising

7 Laboratory tests CBC: WBC: 8.99 (4-11) Hgb: 11.6 (3/2013)-> 10.1 (4/1/2013)-> 8.1 (4/18/2013) Platelets: (3/2013) -> 80(4/18/2013) RDW=17.3 Calcium 7.7 ( ) Phos 2.8 ( ) Glucose 85 Na 143 K 4.6 ( ) CL 106 (98-107) CO2 29 (21-32) LDH 660 (84-246) Haptoglobin 14.1 (30-200) Creatinine 0.77 (3/2013)->1.82 (4/1/2013)->4.69 ( 4/18/2013)

8 Urine analysis with microscopy COLORLatest Range: COLORLESS-YEL. LT YELLOW APPEARANCELatest Range: CLEAR HAZY (A) SP. GRAVITYLatest Range: PH Latest Range: PROTEINLatest Range: NEGATIVE mg/dl 100 (A) GLUCOSELatest Range: NEGATIVE mg/dl NEGATIVE KETONELatest Range: NEGATIVE mg/dl TRACE BILIRUBINLatest Range: NEGATIVE NEGATIVE BLOODLatest Range: NEGATIVE MODERATE (A) NITRITELatest Range: NEGATIVE NEGATIVE UROBILINOGENLatest Range: <2.0 mg/dl NORMAL LEUKOCYTE ESTERASELatest Range: LARGE (A) RBCLatest Range: 0-20 /ul 123 (H) WBCLatest Range: 0-25 /ul 958 (H) SQUAMOUS EPILatest Range: 0-30 /ul 19 HYALINE CASTSLatest Range: 0-5 /ul 0

9 Imaging CT Brain : IMPRESSION: Minimal cerebral atrophy. Moderate chronic small vessel ischemic change. Otherwise negative with no evidence of acute finding. CXR: Bibasilar atelectasis and pleural fluid. Pleural fluid is increased in the left base compared with 11/20/13. Decreased right base pleural fluid. Left anterior chest with CCD with lead tips in right atrium and right ventricle. No other change.

10 CXR

11 Summary 65 y/o female with metastatic breast cancer with hypertensive crisis, new onset renal failure, anemia, thrombocytopenia Volume overload with elevated JVD and chest X ray picture suggestive of vascular congestion UA with proteinuria, hematuria and pyuria

12 Acute Kidney Injury (AKI) The RIFLE criteria consists of various graded levels of kidney injury based upon percent rise in serum creatinine, urine output and outcome measures. Risk: 1.5-fold increase in the serum creatinine or GFR decrease by 25 percent or urine output <0.5 mL/kg per hour for six hours Injury: Twofold increase in the serum creatinine or GFR decrease by 50 percent or urine output <0.5 mL/kg per hour for 12 hours Failure: Threefold increase in the serum creatinine or GFR decrease by 75 percent or urine output of <0.5 mL/kg per hour for 24 hours, or anuria for 12 hours Loss: Complete loss of kidney function (eg, need for renal replacement therapy) for more than four weeks ESRD: Complete loss of kidney function (eg, need for renal replacement therapy) for more than three months

13 AKI definition The AKIN (Acute Kidney Injury Network) criteria are a modification of the RIFLE criteria and include both diagnostic and staging system. Stage 1. Increase in serum creatinine 0.3 mg/dl or 1.5 to 2 fold increase from baseline or urine output less than 0.5 mL/kg per hour for more than 6 hours Stage 2. Increase in serum creatinine >2-3 folds from baseline or urine output less than 0.5 mL/kg per hour for more than 12 hours Stage 3. Increase in serum creatinine >3 fold from baseline or serum creatinine of 4.0 mg/dl with an acute rise of at least 0.5 mg/dl or urine output less than 0.3 mL/kg per hour for 24 hours or anuria for 12 hours.

14 AKI Etiology of AKICauses Pre renal azotemiaPoor fluid intake, fluid loss (vomiting, diarrhea, hemorrhage), NSAIDS, ACEI and ARBS, evidence of volume depletion, heart failure, decreased effective circulatory volume (cirrhosis, heart failure) Sepsis associated AKISepsis, sepsis syndrome, septic shock Ischemia associated AKISystemic hypotension, age, CKD Nephrotoxin associated AKI (endogenous) Rhabdomyolysis, hemolysis, tumor lysis syndrome, multiple myeloma, contrast nephropathy Nephrotoxin associated AKI (exogenous) Tubular injury from medications, interstitial nephritis

15 AKI Etiology of AKICauses Glomerulonephritis/ vasculitisGood Pasteur’s disease, Microscopic polyangitis, granulomatous polyangitis Non drug associated interstitial nephritis Tubuluinterstitial nephritis uveitis syndrome, Legionella infection Thrombotic microangiopathyTTP/HUS Atheroembolic diseaseRecent vascular procedures : cardiac catheterization Post Renal AKIKidney stones, prostate hypertrophy, obstructed bladder catheter

16 Urine sediment

17 Pre renal azotemia Accounts for 40-55% of all cases of acute renal injury Volume responsive- Hemorrhage (traumatic, gastrointestinal, surgical), gastrointestinal losses (vomiting, diarrhea, nasogastric suction), renal losses (overdiuresis, diabetes insipidus), and third spacing (pancreatitis, hypoalbuminemia) Volume unresponsive - Cardiogenic shock, septic shock, cirrhosis, hypoalbuminemia, and anaphylaxis all decrease effective arterial circulating volume, independent of total body volume status, and result in reduced kidney blood flow

18 Pathophysiology Hypoperfusion activates baroreceptors and activates a cascade of neural and humoral responses Increase in antidiuretic hormone and renal adrenergic activity Increase in angiotensin II activity which causes afferent arteriolar constriction that reduces renal plasma flow, GFR, and the filtration fraction, and markedly augments proximal tubular sodium reabsorption in an effort to restore plasma volume Severe and untreated hypoperfusion predisposes the kidney to ischemic acute tubular necrosis (ATN) and nephrotoxic AKI

19 Laboratory studies BUN/Creatinine ratio >20 FeNa <1% Hyaline casts in urine sediment Urine specific gravity >1.018 Urine osmolality >500 mOsm/kg

20 Post renal AKI Upper urinary tract Extrinsic Upper urinary tract intrinsic Lower urinary tract Retroperitoneal space-lymph nodes, tumors NephrolithiasisProstate- BPH, Carcinoma, infection Pelvic or intraabdominal tumors StricturesBladder- calculi, neck obstruction, cancer, infection FibrosisEdemaFunctional Ureteral ligation/surgical trauma Debris, blood clots, sloughed papillae, fungal ball Urethral – posteriors urethral valves, strictures, trauma Granulomatous disease malignancy Hematoma

21 Post renal AKI Accounts for less than 5% of AKI Pain and oliguria are non specific findings

22 Intrinsic AKI

23 Acute Tubular Necrosis (ATN) Ischemic insult causes proximal tubule cell injury and dysfunction Profound drop in GFR through afferent arteriolar vasoconstriction Mediated by tubular glomerular feedback and proximal tubular obstruction Sloughed tubule cells, brush border vesicle remnants and cellular debris in combination with Tamm-Horsfall glycoprotein form the classical muddy brown granular casts

24 ATN Regeneration can occur after removal of the insult Minimally injured cells will repair themselves without dedifferentiation Severely injured cells will undergo dedifferentiation with proliferation of viable cells which spread across the denuded basement membrane and convert back into normal tubular cells

25 Laboratory findings Muddy brown granular or tubular epithelial cell casts FeNa >1% UNa >20 mEq/L Specific gravity ~ 1.010

26 Acute interstitial nephritis (AIN) Systemic allergic response Leukemia, lymphoma, sarcoidosis, bacterial infections, viral infections Rash, fever, eosinophilia, pyuria with eosinophiluria (in NSAID related AIN lymphocytes predominate) Inflammatory infiltrates in interstitium in deep cortex and outer medulla with edema

27 Nephrotoxic AKI The kidneys are vulnerable to toxicity due to their high blood flow, and they are the major route for metabolizing and eliminating drugs and toxins Concentration of drugs within the tubular lumen and the interstitium leads to higher exposure rates

28 Nephrotoxic ATN -AKI

29 Intrinsic AKI

30 Glomerular injury The nephrotic syndrome is defined by the relatively acute onset of edema, nephrotic range proteinuria (defined as greater than 3.5 g/d per 1.73 m2 of body surface area), hypoalbuminemia, hyperlipidemia, and lipiduria, all of which occur with minimal impairment of the glomerular filtration rate (GFR). The acute nephritic syndrome in its full-blown form is characterized by edema; hypertension; azotemia with the variable presence of oliguria; and a ‘‘nephritic’’ urinary sediment marked by the presence of erythrocytes (red blood cells [RBCs]), leukocytes (white blood cells [WBCs]), cellular casts (especially RBC casts), and mild to moderate proteinuria.

31 Acute Nephritic syndrome

32 Ig A nephropathy All age groups might be affected though more common in children and young adults and occurs more often in boys and men Characteristic presentation for IgAN is recurrent episodes of macroscopic hematuria (usually brown in color without blood clots) that may be associated with flank pain and typically coincide with or closely follow an upper respiratory tract infection

33 ANCA associated glomerulonephritis Granulomatous polyangiitis and microscopic polyangiitis Systemic small-vessel vasculitides that typically affect multiple organ systems and are associated with nonspecific features of inflammation, such as fever, malaise,myalgia, arthralgia, and weight loss, with a peak age of onset in the seventh and eighth decades

34 ANCA associated glomerulonephritis The renal features of ANCA-associated vasculitis are oliguria, hematuria, and proteinuria with RBC casts Serum creatinine may or may not be elevated on initial presentation but generally increases rapidly over days to weeks without treatment

35 ANCA associated glomerulonephritis Diffuse pulmonary infiltrates on chest radiographs and a microcytic anemia are suggestive of concurrent alveolar hemorrhage Antibodies directed against proteinase 3 are usually associated with c-ANCA and with GP, whereas antibodies against myeloperoxidase, generally seen in MPA and renal-limited disease, give a p-ANCA pattern

36 Anti- GBM syndrome The disease has two peaks of occurrence, the first in younger men and the second in elderly women, but it can occur at any age and in either sex Extra renal findings- pulmonary hemorrhage, arthralgias, fevers, chills, hepatosplenomegaly Renal presentation is a typical nephritic syndrome

37 Membranoproliferative GN Idiopathic type 1 MPGN is most often seen in adolescents and young adults as a renal-limited disorder presenting with severe proteinuria or nephrotic syndrome and accompanying nephritic features, particularly hematuria and RBC casts Azotemia and hypertension may be present The clinical presentation is similar in adults; however, the disease is usually secondary to a chronic or subacute infectious process, systemic autoimmune disorder, or lymphoma

38 Thrombotic microangiopathy (TMA) Thrombotic microangiopathy (TMA) in the form of Hemolytic uremic syndrome (HUS) and Thrombotic thrombocytopenic purpura (TTP) is a disease of multiple etiologies manifesting as non- immune hemolytic anemia, thrombocytopenia, varying degrees of encephalopathy, and renal failure due to platelet thrombi in the microcirculation of the kidneys

39 Thrombotic microangiopathy HUS develops in children with hemorrhagic colitis from infection by verotoxin-producing Escherichia coli associated with ingestion of undercooked meat Idiopathic TTP is usually seen in adult women with encephalopathy as the predominant clinical feature Both arise from endothelial cell dysfunction and cause a similar clinical and laboratory picture

40 TTP TTP classically manifests with the pentad of thrombocytopenia, microangiopathic hemolytic anemia, fever, neurologic dysfunction, and renal dysfunction Thrombocytopenia is diagnostic; most patients present with values below 60,000/μL

41 Thrombotic microangiopathy Laboratory findings include elevated indirect bilirubin and lactate dehydrogenase levels, depressed serum haptoglobin values, and schizocytes on peripheral blood smear The characteristic renal lesion consists of vessel wall thickening in capillaries and arterioles, with swelling and detachment of endothelial cells from the basement membranes and accumulation of subendothelial fluffy material

42 TMA in cancer patients DrugsImmunosuppressive Agents MalignancyHematopoietic cell transplantation Mitomycin CCyclosporinGastric CaBone marrow transplant nephropathy CisplatinTacrolimusBreast CaRadiation nephropathy BleomycinRapamycinLung Ca Gemcitabine

43 Malignant hypertension Rapidly progressive BP elevations with target organ injury including retinal hemorrhages, encephalopathy, and declining kidney function If untreated, patients with target organ injury including papilledema and declining kidney function suffered mortality rates in excess of 50% over 6–12 months, hence the designation “malignant”

44 Malignant hypertension Renal abnormalities typically include rising serum creatinine and occasionally hematuria and proteinuria Biochemical findings may include evidence of hemolysis (anemia, schistocytes, and reticulocytosis) and changes associated with kidney failure

45 Renal vein thrombosis Renal vein thrombosis (RVT) presents with flank pain, tenderness, hematuria, rapid decline in renal function, and proteinuria Homocystinuria, endovascular intervention, surgery, dehydration, compression and kinking of the renal veins from retroperitoneal processes such as retroperitoneal fibrosis and abdominal neoplasms, antiphospholipid antibody syndrome, nephrotic syndrome, proteins C and S, antithrombin deficiency, factor V Leiden, disseminated malignancy, and oral contraceptives

46 Intrinsic AKI

47 Urine sediment

48 Extra information for diagnosis History h/o chemotherapy h/o infections, fevers OTC medication use Exam Previous BP readings, orthostats Laboratory tests CBC with differential and RBC indices Hepatic function panel with bilirubin Fractional excretion of sodium

49 Differential Diagnosis 1. Thrombotic thrombocytopenic purpura 2. Malignant hypertension 3. Renal vein thrombosis 4. ANCA associated vasculitis 5. ATN- nephrotoxins/ischemic

50 References Taal: Brenner and Rector’s the kidney; 9 th Ed Saunders, an imprint of Elseviers, accessed through MD consult Harrison’s online: Harrison’s principles of Internal Medicine, 18 Ed. Dan L. Longo, Anthony S. Fauci, Dennis L. Kasper, Stephen L. Hauser, J. Larry Jameson, Joseph Loscalzo, Eds. Accessed through Access Medicine Beck, L.H., Salant, D.J. (2008) Glomerular and tubulointerstitial diseases. Primary Care Clinical Office Practice. Vol. 35: 265–296


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