sugar ‘n spice, aint everything nice

Sugar ‘N Spice, Aint Everything Nice

SGD Case 4

History, PE, Laboratory and Ancillary Tests

Sanez, John Ericson T.

60 y/o, male, CC: persistent nausea and vomiting

Sanez, John Ericson T

Physical Exam

• 160/90 mmHg, 81 bpm, 19/min, 39 C• Wt: 83 kg, Ht: 165, BMI 30• Sallow skin, periorbital and facial swelling• Pale palpebral conjuctivae, (+) retinal

hemorrhage and cotton wool spots• Distended neck veins, JVP 5 cm at 30o• Symmetrical chest expansion, (+) intercostal

and subcostal retractions, (+) bibasilar crackles


Physical Exam

• AB at 6th ICS AAL, no heaves, no lifts, no murmurs

• (+) bulging flanks, (+) fluid wave, (+) grade 2 bipedal edema


Complete Blood CountHemoglobin 83 mg/dLHematocrit 0.26WBC 17.5 x 10/L Segmenters 0.79 Lymphocytes 0.19 Monocytes 0.01 Eosinophils 0.01Platelets adequate


UrinalysisColor YellowTransparency Slightly TurbidpH 6.0Specific gravity 1.020Albumin +++Sugar ++Hyaline casts 0-8/csBroad casts 2-6/hpfRBC 0-1/hpfPus cells 1-3/hpfSquamous cells fewAmorphous urates few


Blood ChemistriesUric acid 8.3 mg/dL

BUN 136.1 mg/dL

Serum creatinine 9.3 mg/dL

FBS 109.1 mg/dL

Albumin 2.6 mg/dL

Serum Na+ 130 mEq/L

Serum k+ 5.9 mEq/L

Ionized calcium 1.10 mEq/L

Inorganic phosphorus 7.9 mg/dLSanez, John Ericson T

Urine ChemistriesUrine submitted 24 hrs

Total volume 800 mL

Creatinine clearance 10 cc/min

Serum creatinine 9.3 mg/dL

Urine creatinine 1.6 g/24 hr (20mg/kg/day)

Urine protein 3.5 g/24 hr (<0.15 g/day)


Ultrasound of the Kidney

• Right kidney– 9.7 x 3.9 cm– Cortical thickness 1.1 cm– Increased parenchymal echogenicity

• Left kidney– 9.9 x 3.8 cm– Cortical thickness 1.2 cm– Increased parenchymal echogenicity• No stones, mass, nor structural deformity noted

bilaterally


2. Compute for the estimated renal function using the present serum

creatinine of 9.3 mg/dL.

SALES, Maria Stephanie

Glomerular Filtration Rate• Generally considered the best overall

indicator of the level of kidney function • Any substance X that has the same

concentration in the glomerular filtrate as in plasma, and is neither reabsorbed nor secreted along the nephron, could serve as a glomerular marker for measuring GFR

GFR = sum of volume flow from the plasma into all Bowman's spacesU = urine concentration of the soluteV = urine flowP = concentration of the solute in plasmaP

V x U GFR


Creatinine Clearance

• Clinically used to measure GFR• Creatinine is useful for estimating GFR

because it is a small, freely filtered solute that is endogenously produced

• Serum creatinine levels can increase acutely from dietary ingestion of cooked meat

• Creatinine can be secreted into the proximal tubule, leading to overestimation of the GFR


Creatinine Clearance

(mg/mL)

(mL/min)(mg/mL)(mL/min)

Cr

CrCr

P V x U

C

mg/mL

mL/minmg/mL

093.0 0.56 x 2

mL/min 12


Cockcroft-Gault Method

72 x (mg/dL) P

(kg) weight body x age)-(140 (mL/min)C

Cr Cr

72 x 3.9

83 x )60140(

mL/min 9.9* this value should be multiplied by 0.85 for women, since a lower fraction of the body weight is composed of muscle


MDRD (modification of diet in renal disease)

)( agex )(P x 1.86 GFR -0.203154.1Cr

21.73mper ml/min ee

black)if (1.21 x female)if (0.742 x

Source: http://www.nkdep.nih.gov/professionals/gfr_calculators/orig_con.htm


http://www.nkdep.nih.gov/professionals/gfr_calculators/orig_con.htm

3. What is the gold standard in estimating renal function?


Inulin

• Exogenous starch-like fructose polymer• Fulfills all the criteria for use of a substance to

measure GFR

Criteria for Use of a Substance to Measure GFR

1. Substance must be freely filterable in the glomeruli.

2. Substance must be neither reabsorbed nor secreted by the renal tubules.

3. Substance must be neither metabolized nor produced by the kidney.

4. Substance must be physiologically inert (not toxic and without effect on renal function).


SALES, Maria StephanieSALES, Maria Stephanie

Inulin

• Not a convenient marker for routine clinical testing needs to be injected intravenously

• Problems of intravenous infusion of a GFR marker can be completely avoided by using an endogenous substance with inulin-like properties Creatinine

• In clinical practice, determining the creatinine clearance is an easy and reliable means of assessing the GFR, and such determination avoids the need to inject anything into the patient


6. Tabulate the differences/similarities between acute and chronic renal failure.


Acute Renal Failure Chronic Renal Failure

Etiology • Renal hypoperfusion (prerenal)• Diseases that directly involve the

renal parenchyma (intrinsic)• Urinary tract obstruction

(postrenal)

•Diabetic nephropathy•Hypertensive nephropathy

Important Characteristics

•Anuria, Oliguria•Documented recent decline in GFR

• Azotemia for > 3 months• Prolonged uremic signs and

symptoms• Signs and symptoms of renal

osteodystrophy

History of kidney disease,

hypertension, abnormal urinalysis

Absent Present

Reversibility Usually complete Continuing significant irreversible reduction in nephron number


Acute Renal Failure Chronic Renal Failure

Kidney size Normal Small

Broad casts on urinalysis

Absent Present

Anemia, Metabolic Acidosis,

Hyperkalemia, Hyperphosphatemia

Often present Usually present


DIABETIC NEPHROPATHY

Presenter: Regina Ma. N. San Pedro

Diabetic nephropathy is kidney disease that develops as a result of diabetes mellitus

(DM).

DIABETIC NEPHROPATHYDIABETIC NEPHROPATHY


A clinical syndrome characterized by:

• Persistent albuminuria (>300 mg/d or >200 mcg/min) that is confirmed on at least 2 occasions 3-6 months apart

• A relentless decline in the glomerular filtration rate (GFR)

• Elevated arterial blood pressure.

5 years PTA: 2+ proteinuria5 months PTA: bubbly urineAdmission: albumin +++

5 years PTA: 51mL/min4 months PTA: 30.7mL/minAdmission: 9.9mL/min

Admission: 160/90mmHg

PATIENTPATIENT


STAGES OF DIABETIC NEPHROPATHYSTAGES OF DIABETIC NEPHROPATHY

Source: www.emedicine.medscape.com

STAGES OF CKD (KDOQI)STAGES OF CKD (KDOQI)


STAGE GFR, mL/min per 1.73m2

0 >902 >/= 903 60-894 15-295 <15

Risk factors: HPN, DM, autoimmune disease, older age,

African ancestry, FH of renal disease, previous episode of ARF, presence of proteinuria, abnormal

urinary sediment, or structural abnormalities of the urinary tract

With demonstrated kidney damage (persistent proteinuria, abnormal urine sediment, abnormal blood and urine chemistry, abnormal

imaging studies)


End stage renal disease

Accumulation of toxins, fluid and electrolytes

UREMIC SYNDROME


Impaired host of metabolic and endocrine

functions

AnemiaMalnutrition

Abnormal metabolism of CHO, fats and CHON

Altered plasma levels of hormones

(PTH, insulin, glucagon, sex hormones, prolactin)

UREMIC

SYNDROME

UREMIC

SYNDROME

Worsening systemic inflammation

Elevated CRP

MALNUTRITION-INFLAMMATION-ATHEROSCLEROSIS/CALCIFICATION SYNDROME

9. Therapeutic Plans

SANTOS, Mary Elaine S.

Therapeutic Goals

• To slow the progression of the disease• Treatment of comorbid conditions• Managing complications• Preparation for kidney replacement therapy• Patient education

Slowing the progression of CKD

• Protein Restriction– While protein restriction has been advocated to

reduce symptoms associated with uremia, it may also slow the rate of renal decline at earlier stages of renal disease

– daily protein intake of between 0.60 and 0.75 g/kg per day

• Reducing Intraglomerular Hypertension and Proteinuria

– 125/75 mmHg– ACE inhibitors and ARBs

• inhibit the angiotensin-induced vasoconstriction of the efferent arterioles of the glomerular microcirculation.

Slowing the progression of CKD

Slowing progression of Diabetic Renal Disease

• Control of Blood Glucose– Preprandial glucose = 5.0–7.2 mmol/L (90–130

mg/dL)– Hgb A1C = < 7%– As the GFR decreases with progressive

nephropathy, the use and dose of oral hypoglycemics needs to be reevaluated.

– As renal function declines, renal degradation of administered insulin will also decline, so that less insulin may be required for glycemic control.

• Control of Blood Pressure and Proteinuria

– Antihypertensive treatment reduces albuminuria and diminishes its progression.

– In addition to treatment of hypertension in general, the use of ACE inhibitors and ARBs in particular is associated with additional renoprotection.

Slowing progression of Diabetic Renal Disease

Managing other complications of CKD

• Hyperphosphatemia– low-phosphate diet – use of phosphate-binding agents

• taken with meals and complex the dietary phosphate to limit its GI absorption

• E.g. calcium acetate, calcium carbonate

• Hypertension– blood pressure should be reduced to 125/75– Salt restriction and diuretics are first line therapy– ACE inhibitors and ARBs

• slow the rate of decline of kidney function

• Anemia– target a hemoglobin concentration of 110 to 120

g/L– recombinant human EPO and modified EPO

products– oral iron supplementation– vitamin B12 and folate

Managing other complications of CKD

Preparation for Renal Replacement Therapy

10. What are the most common causes of chronic renal failure in the

USA? Philippines? SANTOS, Mary Elaine S.

National Kidney Foundation (www.kidney.org) Philippine Renal Disease Registry Annual Report in 2008

http://www.kidney.org/

sugar ‘n spice, aint everything nice

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