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Morning Report Jieli Li 03/28/05. Chief Complaint  Generalized edema x 1 week.

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Presentation on theme: "Morning Report Jieli Li 03/28/05. Chief Complaint  Generalized edema x 1 week."— Presentation transcript:

1 Morning Report Jieli Li 03/28/05

2 Chief Complaint  Generalized edema x 1 week

3 HPI  46 y/o AAM with hx of htn, Hep C, syphillis presented to Urgent Care with generalized edema x 1 week  Pt noticed progressive lower extremity edema, then scrotal edema, as well as tightness in abdomen. + facial edema as well  Pt was seen by PMD and started on HCTZ last week without any relief

4 HPI cont.  + 2 pillow orthopnea  + 1 episode of PND and wheezing recently  + occasional wheezes x 1 yr  + SOB with exertion  + occasional cough with yellow phlegm  Baseline exercise capacy excellent  No CP, f/c/s, no diarrhea/constipation  No dysuria, no hemauria

5 PMH  Htn – dx’d 1 yr ago  Hep C – never treated  Syphillis – treated in 1989  Depression  Hyperlipidemia  Bilateral leg fractures in the past

6 Meds & Allergies  Meds: Atenolol 50 qd HCTZ 12.5 qd Simvastatin 10 qhs Ascorbic acid 500 qd Alleve prn (OTC)  Allergy: NKDA

7 Social and Family History  SH: Single, lives at Midnight Mission Hx of incarceration x 37 months until Nov 2004, HIV neg in 2000 Hx of cocaine, MJ, no IVDU Hx of heavy etoh use, quit 40 months ago Hx of tobacco (1/2 pk per day x 20 yrs), quit 2 yrs ago  FH: Mother: DM & htn Father: CAD with triple bypass

8 Physical Exam  VS: 96.8, 73, 20, 178/99, 0/10  Gen: obese AAM with anasarca, NAD, AAO x 4  HEENT: PERRLA, EOMI, op moist and intact, no lesions  Heart: distant heart sounds, no murmurs appreciated  Lungs: cta bilaterally, no crackles/wheezes  Abd: obese, mildly distended, NT, na bs, no hsm

9 PE cont.  GU: + large scrotal edema, non-tender, testes palpable and intact, no masses  Ext: 2-3+ pitting edema bilateral legs, generalized anasarca, + patchy flesh-colored papular lesions bilateral shins, faint pulses bilaterally

10 Lab Studies  UA Spec grav 1.04 PH 6.5 Protein > 600 Glucose neg Ketones neg Bilirubin neg Small occult blood Urobilinogen 0.2  Spot protein/Cr: 2967/396 = 7.5  24 hr urine protein: 12.1g Nitrite neg LE neg RBC 4 WBC 8 Hyaline casts 40

11 Lab Studies cont Alk Phos 66 ALT 14 Total bili 0.7 Alb 1.1 Total cholesterol 411 Trig 157 HDL 121 LDL 259

12 Glomerulonephritis Panel  RPR 1:1  MHA-TP: 4+  ESR: 89  HIV neg  C3 and C4: nl  RF: neg  ASO: nl  SPEP: hypogammaglobulinemia  Cryoglobulin neg  Hep A ab R, IgM NR  Hep B surface Ag NR  Hep B core Ab NR  HCV RNA 1,010,000  HIV neg

13 Renal u/s  Right kidney 14.6 cm, left kidney 13 cm  No definitive abnormalities although there is very mild increased cortical echogenicity  Mildly enlarged prostate without bladder outlet obstruction

14 Hospital Course  Pt was admitted to GMED for workup of his nephrotic syndrome  Hep C induced MPGN vs FSGS vs membranous GN was high on the differential  Pt was started on lasix, titrated up to 40 po bid eventually for his anasarca  He was placed on low salt diet  ACEI was held during diuresis, Cr improved to baseline (1.1)

15 Hospital Course cont.  GI was consulted for possible Hep C treatment after HCV RNA came back > 1 million  Pt’s proteinuria was followed by serial protein/Cr ratio and 24 hr urine protein  Renal biopsy showed minimal change disease confirmed by EM  This was believed to be 2/2 hx of NSAIDS  By the time of discharge, pt has only trace protein on UA, he did not receive any further tx

16 1 week follow up  At the renal clinic f/u one week after discharge, pt’s proteinuria has dropped from 12 g/day to 0.3 g/day. He has lost nearly 100 lbs on diuresis (back to baseline wt). He is no longer taking NSAIDs.

17 Nephrotic Syndrome  Defined by presence of: heavy proteinuria (> 3g/24hrs) Hypoalbuminemia (< 3.0 g/dL) Peripheral edema  Isolated heavy proteinuria is more likely to be due to secondary focal glomerulosclerosis  Urinary sediment: few cells or casts Lipiduria (oval fat bodies)

18 Oval Fat Bodies

19 Etiology  In children Minimal change disease is predominant  In adults Systemic disease related: 30% Primary renal disorders: 70%  Membranous nephropathy  Focal glomerulosclerosis  Minimal change disease  Amyloidosis  In elderly Increased incidence of amyloidosis and decreased incidence of SLE

20 Etiology cont.  Although nephrotic syndrome can develop in patients with postinfectious GN, membranoproliferative GN, and IgA nephropathy, most commonly these disorders present with a “nephritic” picture, i.e., RBC and cellular casts in UA

21 Minimal Change Disease  90% of nephroitic syndrome in children under the age of 10  50% of cases in older children  In adults, can occur as an ideopathic condition or be associated with: NSAIDs Cancers as a paraneoplastic phenomenon, most often Hodgekin’s Disease

22 Minimal Change Disease  Light Microscopy Either normal or reveals only mild mesangial cell proliferation  EM Diffuse fusion of the epithealial cell foot processes

23 Minimal Change Disease

24 Focal Glomerulosclerosis (FGS)  35% of all cases of nephrotic syndrome in the U.S.  > 50% of cases among African Americans  Can occur as an ideopathic condition or be associated with: HIV disease reflux nephropathy Healed previous glomerular injury NSAIDs Massive obesity

25 Diagnostic Considerations for FGS  Sampling error in renal biopsy may lead to misclassification of FGS as minimal change disease  Steroid-resistance in minimal change disease pts should raise suspicion for FGS  Primary FGS usually presents with acute onset nephrotic syndrome, tx is corticosteroids.  Secondary FGS usually presents with slowly increasing proteinuria, nephrotic syndrome is rare. Tx is ACEI.

26 Focal Glomerulosclerosis

27 Collapsing FGS  A histologic variant usually associated with HIV infection  Tendency to collapse and sclerosis of the entire glomerular tuft, rather than segmental injury  Often severe tubular injury with proliferative microcyst formation and tubular degeneration  Often with rapidly progressive renal failure  Optimal therapy is uncertain

28 Collapsing FGS

29 Membranous Nephropathy  Basement membrane thickening with little or no cellular proliferation or infiltration  Presence of electron dense deposits across the glomerular basement membrane  Can occur as ideopathic condition or be associated with: Hep B Autoimmune diseases Thyroiditis Carcinoma Certain drugs (e.g., gold, penicillamine, captopril and NSAIDs)

30 Membranous Nephropathy

31 Amyloidosis  4-17% of nephrotic syndrome  Increased frequency among elderly  Two major types: Primary amyloid (AL)  A light chain dyscracia  Fragments of monoclonal light chains form the amyloid fibrils Secondary amyloid (AA)  Acute phase reactant serum amyloid A forms the amyloid fibrils  Assoc with chronic inflmmatory diseases such as RA or osteomyelitis

32 Amyloidosis

33 Pathophysiology  Proteinuria Increased filtration of macromolecules across the glomerular capillary wall Commonly due to abnormalities in podocytes Increased loss of:  Albumin  Clotting inhibitors  Transferrin  Hormone binding proteins (e.g., Vit D binding protein)

34 Pathophysiology  Hypoalbuminemia Presumably 2/2 proteinuria Unclear why hepatic synthesis can not compensate sufficiently  Edema Marked hypoalbuminemia leading to movement of fluid into the interstitial space by decreasing plasma oncotic pressure Primary renal sodium retention in collecting tubules

35 Pathophysiology  Hyperlipidemia and lipiduria Decreased plasma oncotic pressure stimulates hepatic lipoprotein synthesis Diminished clearance may also play a role Impaired metabolism is primarily responsible for nephrotic hypertriglyceridemia Oval fat bodies are thought to be degenerated renal tubular epithelial cells containing cholesterol esters

36 Complications of Nephrotic Syndrome  Protein malnutrition  Hypovolemia  Acute renal failure  Urinary loss of hormones  Hyperlipidemia and the potential for accelerated atherosclerosis  Thrombosis  Increased susceptibility to infection

37 Protein malnutrition  Loss in lean body mass due to proteinuria  May be masked by concurrent edema  May be compounded by GI symptoms of anorexia and vomiting 2/2 bowel edema

38 Hypovolemia  Often as a result of overdiuresis in those with a serum albumin < 1.5 g/dL  Occurs more often in children

39 Acute Renal Failure  Can be seen in: Minimal Change Disease Collapsing FGS Crescentic glomerulonephritis superimposed upon membranous nephropathy  Mechanism not well understood Hypovolemia Interstitial edema Ischemic tubular injury NSAIDs

40 Thromboembolism  Increased incidence of arterial and venous thromboemboli, particularly DVT and renal vein thrombosis  Mechanism not well understood  Renal vein thrombosis is most often found with membranous nephropathy Can present acutely with flank pain, gross hematuria and ARF or Indolent disease without symptoms, suspected only when PE occurs

41 Infection  Before abx became available, this used to be the leading cause of death in children with nephrotic syndrome  Pneumococcal infections, esp peritonitis were most common  Mechanism is not well understood Low levels of IgG may play a role

42 Proximal tubular dysfunction  Often associated with advanced disease  Can result in: Glucosuria Aminoaciduria Phosphaturia renal tubular acidosis Vitamin D deficiency Thyroid dysfunction – due to loss of thyroxine- binding globulins

43 Diagnosis  24 hour urine collection > 3 g/day  Total protein to creatinine ratio on spot urine specimen Correlates with daily protein excretion in g/1.73 m2 of body surface area  In history, should look for hx of DM, SLE, HIV, drugs such as NSAIDs, gold, penicillamine

44 Serologic Studies  Certain serologic tests may preclude the need for renal biopsy: SPEP/UPEP  Presence of a paraprotein should be followed by fat pad or rectal biopsy to look for amyloidosis ASO  poststreptococcal glomerulonephritis Cryoglobulins  Mixed cryoglobulinemia, commonly 2/2 Hep C

45 Renal Biopsy  In adults, renal biopsy is usually required to determine diagnosis  Contraindications: Uncorrectable bleeding diathesis Uncontrolled hypertension Small kidneys generally indicative of chronic irreversible disease Multiple bilateral cysts or renal tumor Hydronephrosis Active renal or perirenal infection Uncooperative patient

46 Management  Proteinuria ACEI / ARB  To lower intraglomerular pressure, which may reduce protein excretion and slow the rate of disease progression  Potential adverse effects include ARF and hyperkalemia Evidence is unclear on protein restriction

47 Management  Edema Dietary sodium restriction  Edema is due to primary renal sodium retention in most cases Diuretics  Proceed slowly to prevent acute hypovolemia  Generally there is lesser natriuresis than in normal patients because of hypoalbuminemia and albuminuria  Serial body weight is important in guiding the titration of diuretics

48 Management  Hyperlipidemia Usually reverse with resolution of the renal disease In case of persistent nephrosis, dietary modification is usually of little value and a statin is usually required  Hypercoagulability Some have suggested prophylactic anticoagulation in membranous nephropathy due tot high incidence of thromboemboli In others, if unexplained thrombosis occurs, they should be put on heparin followed by warfarin for as long as the nephrotic syndrome persists


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