Ministry Saint Joseph’s Hospital
Clinical Case Study
Presented by: Jolene Sell,
Keene State Dietetic Internship 2012-2013
• Founded more than 100 years ago
• The only major rural referral medical center in
Wisconsin providing health care to Wisconsin and
Upper Michigan
• 500+ bed tertiary care teaching institution
• 8 Regular Clinical Registered Dietitians, 4 DTRs
Objectives
 Understand the physiology of the kidney
 Discuss the pathophysiology of IgA nephropathy and
Chronic Kidney Disease Stage 3
 Determine medical diagnosis and treatment
 Case study patient
 Nutrition Care Process
 MNT Recommendations
Physiology of the Kidney
Normal GFR over 90mls/min/1.73m2
Pathophysiology of IgA
Nephropathy
 IgA Nephropathy (Berger’s disease)
 Most common lesion found to cause primary
glomerulonephritis throughout most developed countries.
 Autoimmune renal disease arising from consequences of
increased circulating levels of IgA
 Initiating event is the mesangial deposition of IgA
 Etiology
 Unknown-possibly dysregulation synthesis and metabolism of
IgA
 Environmental factors are a possibility
 Dietary antigens and mucosal infections
BRIEF REVIEW
www.jasn.org
Hit 1
Hit 2
Increased circulating
galactose-deficient IgA1
Production of unique
anti-glycan antibodies
Hit 3
Formation of pathogenic IgA1-containing
circulating immune complexes
Hit 4
Mesangial deposition and activ ation of
mesangial cells resulting in glomer ular injury
Proliferation
ECM production
Cytokines
Growth factors
Mesangial cell
IgA1 complexes
Cytokines
Pod
Podocyte
Figure 2. Proposed pathways involved in the pathogenesis of IgAN: multi-hit mechanism.
Hit 1: Production of galactose-deficient IgA1 by a subpopulation of IgA1-secreting cells. IgA1
production may be affected by the IgAN-associated locus on chromosome 22q12.2.3 Hit 2:
ing healthy individuals and patient
wi th H enoch-Schoenlei n purpur
without nephritis. 19,24,25 The com
plexes i n pati ents wi th Henoch
Schoenlein purpura without nephriti
consist of IgA, but not IgG, and are o
smaller massthan thecomplexesfoun
in patientswith IgAN. Asthese person
do not develop overt renal disease,
can be assumed that these IgA com
plexes are not nephritogenic. In con
trast, patientswith Henoch-Schoenlein
purpura with nephritis have larger cir
culating immune complexes contain
ing IgA and IgG.24 By analogy wit
other human diseases caused by im
mune complexes, it is likely that, i
IgAN, the molecular proportion of an
tigens (galactose-deficient IgA1) an
antibodies (IgG or IgA1) determine
the size of the formed immune com
plexes and, consequently, their rate o
removal from thecirculation, aswell a
biologic activity. Thepathogenic circu
lating IgA1-IgG immune complexes i
patients with IgAN are relatively larg
( 800 kD) and thus may be exclude
from entry into the hepatic space o
Disse to reach the asialoglycoprotein
receptor (ASGP-R) on hepatocytes, th
normal catabolic pathway for circula
tory IgA1. As a result, these immun
complexes enter the renal circulation
Due to the unique location of the mes
angium between the fenestrated endo
thelial lining of the capillaries and th
glomerular basement membrane, th
mesangium is prone to deposition o
immune complexes. While it is no
completely understood what deter
mines the entry of circulating immun
IgA Cont.
 Risk factors for developing this condition include:
 Ethnicity: More common in Caucasians and Asians than in
African Americans
 Family history: Some cases IgA runs in families
 Diagnosed
 Urine test
 Blood Test
 Kidney biopsy
 Complications
 High blood pressure, high cholesterol, acute and chronic
kidney failure, nephrotic syndrome.
IgA Cont.
 Treatment
 When kidneys are damaged they are not repaired
 Focus is to slow the disease
 One complication is hypertension
 ACE
 ARB’s
 Lowering cholesterol may slow kidney damage
 Statin therapy
 Omega-3s
 Vitamin E
 Corticosteroids (prednisone)
Pathophysiology of CKD 3
 Chronic Kidney Disease
 Slow gradual loss of kidney function.
 Stage 3 CKD: There is a mild decrease in GFR (30-59
mL/min)
 Microalbuminuria becomes consistent and can range from
30-300mg/day starting out
 Uremia occurs as the kidneys function decreases.
CKD Stage 3 Cont.
 Etiology: Diabetes is the leading cause, uncontrolled
hypertension
 Complications:
 High blood pressure, anemia and early bone disease.
 Risk Factors
 Proteinuria, hypertension, dyslipidemia, anemia, oxidative
stress, infections, depression, hyperglycemia, bone
disease, and obesity
CKD Stage 3 Cont.
 Nutrition Status
 Patients are often malnourished due to lack of energy
and appetite due to uremia. Edema occurs and can
further decrease appetite
 Anemia occurs due to the kidney’s inability to make
erythropoietin.
 Vitamin D and calcium status decline
MNT
 Consume adequate calories
 Nondialyzed patients >60 years of age with GFR <25 mL/min need 35kcal/kg/d,
those older than 60 years need 30-35 kcal/kg/d
 Carbohydrates should be 50-60% of total calories
 Stages 1,2 or 3 of CKD limit protein to 0.8-1.0g protein per Kg from high
biological value sources
 With diabetes or heart disease, limit total fat to 30% or less of total calories
per day; saturated fat less than 10% of the total calories
 200 mg cholesterol
 Medications: ACE inhibitor, Insulin, iron supplement, lipid lowering
medication, phosphate binders, vitamin supplement, and vitamin D
Case Study Patient
Ms. KT
 Admitted July 22, 2013 with CKD stage 3,
superimposed preeclampsia, gestational diabetes,
intrauterine pregnancy.
1/23/13
 Nephrology Follow-up appointment
 Proteinuria, elevated serum creatitine, possible
microscopic hematuria
 No evidence of nephritic syndrome
 Renal biopsy in patients best interest
 Patient has no plans of becoming pregnant
 No history of diabetes, hypertension, or dyslipidemia
4/08/13
 Patient was referred to a registered dietitian with a diagnosis of
gestational diabetes
 Intervention
 Estimated nutrient needs 1800 calories per day (25
kcal/kg pre-pregnancy ABW per day plus 300 calories per
day to meet pregnancy needs)
 Meal plan
 Breakfast: 30gms CHO
 Lunch: 45 gms CHO
 Snack: 30 gms CHO
 Supper: 45 gms CHO
 Snack: 30 gms CHO
5/09/13
 Follow-up gestational diabetes visit with another RD
 It does not seem that she has been measuring her foods,
reading food labels or complying with this meal plan.
 She also has not been checking her blood sugar. At most she
is checking twice per day. Also not keeping a food log or
journal.
 5-day blood glucose levels. All post-meal glucose levels are within
normal limits. The two available fasting levels are high.
Nephrology Appointment
7/17/13
 7/15/2013
 Protein-Urine, 24 hr
 4922 mg H
 Ms. KT was seen from Nephrology
 Blood pressure running high
 4.9 grams of protein in urine with in a 24 hour period
 Chronic Renal Disease in third trimester
 Possibly IgA nephropathy
 At risk for preeclampsia
7/18/13
 Perinatal Consultation
 Indication: CKD and possibly developing superimposed
preeclampsia
 Unable to have renal biopsy
Admission: 7/22 Day 1
 34 year old female, pregnant 33 5/7 weeks gestation,
EDD 9/5/13
 Admitted with CKD stage 3, superimposed
preeclampsia, gestational diabetes, intrauterine
pregnancy.
 Gravid: 11 Para: 7; 6 full-term deliveries, 1 pre-term
delivery, and 3 miscarriages
 Maternal Vital Signs:
 Blood Pressure: 110-155/63-89
TP
Alb LDH
5.3 L 2.6 L 246H
ALT
AST
eGFR
BUN
Creat
UricA
Gluc
42
49 H
46.6 L
30 H
1.3 H
9.5 H
98-123
Past Medical History
 PMH includes :






Iron deficiency anemia
Renal issues since 2000
Migraine headaches
Anxiety, multifactorial
Obesity
Seasonal allergies
 Food Allergies: Shrimp and crab
Weight Trend
 Pre-pregnancy weight: 187 lbs., 85 kg
 Today’s weight 7/22/13: 197 lbs., 89.5 kg
 Computed pregnancy weight gain 10 lbs.
 Height: 61 inches
 Pre-gravid BMI: 35.4
 Recommended weight gain 11-20lbs
Social and Family History
 Social History:
 Works as a CNA at a nursing home
 Marital Status: Single
 Support person: Boyfriend
 Family History
 Denies and family members with intellectual disabilities,
recurrent pregnancy losses, chromosomal/genetic
disorders or birth defects.
 Denies smoking, alcohol or drug use.
Diet History
 Following Asian Diet: boiled chicken, white rice,
vegetables (broccoli, collard greens, cauliflower,
zucchini)
 Pre-pregnancy: One meal per day consisting of
chicken/pork, white rice, and vegetables
 Since pregnancy 2-3 meals per day, no snacks
Day 2 Chart 7/23
 Nutrition Assessment
 Weight: 194 lbs., 88.2 Kg (-2.9 lbs. from admission)
 Maternal Vital Signs
 Blood Pressure: 104/69-122/80
 Labs
TP
Alb
ALT
AST
eGFR
BUN
Creat
UricA
Gluc
5.0 L
2.5 L
35
34
46.6 L
37 H
1.3 H
9.1 H
91-142
 Nutrition Diagnosis: Food-and Nutrition-related
knowledge deficit related diabetic carbohydrate
controlled diet order as evidenced by education patient
on choosing adequate carbohydrates choices for meals
 Nutrition Intervention
 Issued consistent carbohydrate diet handout
 Issued carbohydrate snack list
 Recommended calorie needs 1800-1900
 Protein 71-82 grams
 Nutrition Monitoring and Evaluation
 Monitor blood sugars and adjust carbohydrate choices as
needed, monitor pertinent labs and weight trend
Day 4
Chart 7/25
 Weight: 84.9 Kg (-10.2 pounds from admission)
 Maternal Vital Signs
 Blood Pressure
 118/71-127/76
 24 Hour Protein-Urine Test
 1265 H
 Creatitine Clearance
 61.2 L
Hgb
6.8 LL
Alb
_
ALT
AST
eGFR
BUN
Creat
40
44 H
42.8 L
30 H
1.4 H
UricA
_
Gluc
99-145
Day 5 Chart 7/26
 Nutrition Assessment Follow-up
 Maternal Vital Signs
 Blood Pressure: 100/66-116/73
 Labs
Hgb
TP/Alb
ALT
8.5 L
5.0L/2.5 L 45
AST
eGFR
BUN
Creat
UricA
Gluc
51 H
42.8 L
28H
1.4 H
10.2 H
83-142
 Nutrition Diagnosis: Inadequate oral food and beverage
intake related to weight loss as evidenced by patient
consuming 900-1200 calories per day per CBORD.
 Nutrition Intervention
 Encouraged appropriate carbohydrate snacks, increased
protein and calorie supplements
 Patient declined all
 Discussed family is able to bring in meals
 Patient is taking PNV and Fe
 Nutrition Monitoring and Evaluation
 Monitor blood sugars and adjust carbohydrate choices as
needed, monitor pertinent labs and weight trend
Day 6 7/27
 Monitor pertinent labs: HELLP Syndrome
 H=hemolysis: breakdown of red blood cells, losing blood
in urine
 EL=elevated liver enzymes
 LP=low platelets
TP
Alb
5.3 L 2.6 L
ALT /LDH
AST
eGFR
BUN
Creat
UricA
GLuc
87 H/229
H
101 H
46.6 L
27 H
1.3 H
10.5 H
84-116
Baby Girl Born
 34 3/7 weeks
 Birth Admit to NICU: Premie
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Weight: 5 lbs. 4.2 ounces
Length: 19 inches
OFC: 31.5 centimeters
Appropriate Gestational Age (AGA)
Discharge plans
 7/30/13
 Labs are stable
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Creatitine 1.2
ALT 112
AST 84
Will have post-partum follow up in 2 weeks
Patient encouraged to make follow up with nephrology
Follow up with the RD for Gestational DM Post Partum
management.
Questions/Co
mments
???
Thank You!
References
 Escott-Stump, S. Nutrition and diagnosis-related care. 7th
ed. Lippincott Williams & Wilkin; 2012.
 Barratt, J. & Feehally, J. Pathogenesis of IgA nephropathy.
In UpToDate, 2013.
 Hitoshi S, Kiryluk K, Novak J, et al. The pathophysiology of
IgA nephropathy. Journal of American Society of
Nephrology. 2011: 1075-1803.
 Curtain WM, Weinstein L. A review of HELLP syndrome.
Journal of Perinatology. 1999: 138-143.
 Cheng YW, Caughey AB. Gestational diabetes: diagnosis
and management. Journal of Perinatology. 2008:657-664.