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Morning Report

Morning Report. Jieli Li 03/28/05. Chief Complaint. Generalized edema x 1 week. HPI. 46 y/o AAM with hx of htn, Hep C, syphillis presented to Urgent Care with generalized edema x 1 week

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Morning Report

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  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. Nitrite neg LE neg RBC 4 WBC 8 Hyaline casts 40 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

  11. 15.2 8.6 356 44.8 141 106 27 93 4.57 31.6 1.4 Alk Phos 66 ALT 14 Total bili 0.7 Alb 1.1 Total cholesterol 411 Trig 157 HDL 121 LDL 259 Lab Studies cont.

  12. 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 Glomerulonephritis Panel

  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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