Management Of Nephrotic Syndrome
Objectives
To briefly review the definition & etiology of nephroticsyndrome.
To understand the terminology pertaining to clinical course of nephroticsyndrome.
To understand the management of nephroticsyndrome:Specific management & Supportive care and management of complications
Management of congenital nephrotic syndrome
Management Of Nephrotic Syndrome
Objectives
To briefly review the definition & etiology of nephroticsyndrome.
To understand the terminology pertaining to clinical course of nephroticsyndrome.
To understand the management of nephroticsyndrome:Specific management & Supportive care and management of complications
Management of congenital nephrotic syndrome
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Similar to Chronic kidney disease in children (20)
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Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
2. INTRODUCTION
• Chronic kidney disease (CKD) refers to a state of irreversible kidney
damage and/or reduction of kidney function that is associated with
progressive loss of function over time.
DEFINITIONS AND CLASSIFICATIONS
3. There are two pediatric exceptions:
(1) the criteria for duration longer than 3 months does not apply to
infants younger than 3 months, and
(2) the glomerular filtration rate (GFR) criteria of less than 60
mL/min/1.73 m2 cannot be used in children under 2 years of age since
developmental immaturity in this age group is associated with mean GFR
of less than this value. Thus, the diagnostic criteria for reduced GFR in
this particular population must be compared to age-matched normative
values.
• Modified Schwartz = 0.413 × length in cm
Serum creatinine in mg/d
The normal GFR in children is 90 - 130 ml/min/1.73m
2
4. CKD is divided into 5 stages according to GFR ( NKF KDOQI GIUDELINES )
GFR
mL/min/1.73 m2DescriptionStage
More than 90
Slight kidney damage with
normal or increased filtration
G 1
60-89
Kidney damage with Mild decrease in
GFR
2
30-59Moderate decrease in GFR3
15-29Severe decrease in GFR4
Less than 15 or in dailysis
Kidney failure; requiring
dialysis or transplantation
5
5. CKD is divided into 5 stages according to GFR:
GFR
mL/min/1.73 m2DescriptionStage
More than 90
Slight kidney damage with
normal or increased filtration
G 1
60-89
Kidney damage with Mild decrease in
GFR
2
30-59Moderate decrease in GFR3
15-29Severe decrease in GFR4
Less than 15 or in dailysis
Kidney failure; requiring
dialysis or transplantation
5
6. ETIOLOGY
in children <5 yr old is most commonly a
result of congenital abnormalities of the
kidney and urinary (CAKUT) such as renal
hypoplasia, dysplasia, or obstructive
uropathy
Additional causes include :-
congenital nephrotic syndrome, prune belly
syndrome, cortical necrosis, focal segmental
glomerulosclerosis,
autosomal recessive PCKD , HUS.
renal vein thrombosis,
After 5 yr of age, acquired diseases (various
forms of glomerulonephritis – FSGS -lupus
nephritis) and inherited disorders (familial
juvenile nephronophthisis, Alport
syndrome).
CKD
related to metabolic disorders
(cystinosis, hyperoxaluria)
9. Pathophysiology of CKD
MECHANISMSMANIFESTATION
Decrease in glomerular filtration rateAccumulation of nitrogenous waste
products
Impaired bicarbonate reabsorption
Impaired ammonia synthesis
Decreased net acid excretion
Metabolic Acidosis – Normal AG or
ed AG
Excessive renin production
Oliguria
Sodium retention
Solute diuresis
Tubular damage
Sodium wasting
Solute diuresis
Tubular damage
Urinary concentrating defect
10. MECHANISMSMANIFESTATION
Decrease in glomerular filtration rate
Metabolic acidosis- extracellular shift of K+
Excessive potassium intake
Hyporeninemic hypoaldosteronism
Hyperkalemia
Impaired renal production of 1,25-
dihydroxycholecalciferol
Hyperphosphatemia
Hypocalcemia
Secondary hyperparathyroidism
Renal osteodystrophy – high turnover
most common 2 to hyperparathyroidism
Inadequate caloric intake
Renal osteodystrophy
Metabolic acidosis
Anemia
Growth hormone resistance
Growth retardation
11.
12. MECHANISMSMANIFESTATION
Decreased erythropoietin production- stage 3-4
Iron deficiency
Folate deficiency
Vitamin B12 deficiency
Decreased erythrocyte survival
Chronic blood loss from uremia-induced platelet
dysfunction .
Chronic inflammation
Secondary hyperparathyroidism- BM fibrosis
Accumulation of inhibitors of erythropoiesis
Anemia- normocytic normochromic anemia with
no reticulocyte response
Defective granulocyte function
Impaired cellular immune functions
Indwelling dialysis catheters
Infection
13.
14. MECHANISMSMANIFESTATION
Gastroesophageal reflux
Decreased gastrointestinal motility
Serositis to uremia
Gastrointestinal symptoms (feeding intolerance,
abdominal pain)
Volume overload
Excessive renin production
Hypertension
Decreased plasma lipoprotein lipase activity-
uremia inhibits lipoprotein lipase and hepatic lipase leads to lack od
degradation of lipids .
Hyperlipidemia
Uremic factor(s)
Hypertension
Fluid overload
Pericarditis, cardiomyopathy
Tissue insulin resistanceGlucose intolerance
15. The goals of therapy in children with CKD are:
1. Treat reversible kidney disease
2. Slow progression to ESRD
3. Manage complications
4. Prepare for RRT- in whom renal replacement therapy will be required
MANAGEMENT
Multidisciplinary Services : Medical , Nursing , Social service Nutritional
Psychological
16. Slowing the progression of kidney dysfunction
1) Optimum Control of Hypertension
2) Control of proteinuria
3) Serum Phosphorus within normal range
4) Serum Calcium-Phosphorus Product < 5 mmol2
/l2
5) Prompt treatment of infectious complications and dehydration
6) Correction of anemia
7) Avoidance of cigarette smoking
8) Minimization of regular use of NSAIDs
9) Control of hyperlipidemia
10)Dietary Protein restriction
17. Dietary Management
Goals –
a) Reduce nitrogen intake
b) Maintain nitrogen balance
c) Cover essential amino acid requirement
d) Supply enough calories
Energy: Intake equivalent to the RDA of healthy children of the same age
• Infant : 100 – 120 kCal/kg/day
• Children : 80 – 100 kCal/kg/day
• 55 – 60% from carbohydrates
• 30% from fats
• 10% from proteins Proteins of high biological value or ‘good quality’ are preferred (are
metabolized primarily to usable aminoacids rather than to nitrogenous wastes) and are found
mainly in eggs, milk, meat, fish and poultry.
Nutrition
18.
19.
20. Anemia become manifested at a GFR less than 35 ml/min/1.73 m2
ESA- Recombinant Human Erythropoietin((Epogen, Procrit, Eprex) is
usually initiated when the patient's Hb concentration falls bellow 10 g/dL ,
at a dose of 50 – 100 unit/kg S.C. one to three times weekly.
An alternative option to rHuEPO is darbepoetin alfa (Aranesp), a longer-
acting agent administered at a dose of 0.45 μg/kg/wk. The chief advantage
of this agent is that it may be dosed once weekly to once monthly because
of its extended duration of action.
• Iron supplementation :- Oral or Intravenous.
oral : 3 – 5 mg/kg/day of elemental iron(max 150 – 300 mg/day)
ANAEMIA
21. • Control of levels of blood phosphate – most important factor in
prevention & treatment of secondary hyperparathyroidism .
• The target phosphorus level for adolescents is between 3.5 and 5.5 mg/ dL,
children 1-12 yr of age it is 4-6 mg/dL ,
Children and adolescents should follow a low-phosphorus diet .
The cornerstone of therapy for renal osteodystrophy is vitamin D administration.
– Therapy may be initiated with 0.01-0.05 µg/kg/24 hr of calcitriol.
– Phosphate binders: • Calcium salts [calcium carbonate & calcium acetate]
• Sevelamer hydrochloride
CKD - MBD
22. Hypertension
ACE inhibitors are the antihypertensive medication of choice in all children with proteinuric
renal disease.
Angiotensin-II blockers have been shown to be effective in controlling BP and in slowing
disease progression in patients with diabetic nephropathy.
23. –Sodium bicarbonate tablets ( 650mg =8meq ) is used to maintain the
serum bicarbonate level above 22 mEq/L.
– Growth problems (especially short stature) are very commen in CKD
children.
– CKD children have an apparent growth hormone resistant state with
elevated GH levels but decreased insuline-like growth factor-I (IGF-I).
Acidosis
Growth problems
24.
25.
26. Long-term Follow Up
close monitoring of a patient's clinical and laboratory status
Blood studies to be followed routinely include:
serum electrolytes
blood urea nitrogen (BUN)
creatinine
calcium
phosphorus
albumin
alkaline phosphatase
Hb and Htc
Periodic measurement of intact parathyroid hormone (PTH) levels and
roentgenographic studies of bone may be of value in detecting early evidence of
renal osteodystrophy
Echocardiography should be performed periodically to identify left ventricular
hypertrophy and cardiac dysfunction that can occur as a consequence of the
complications of CKD
27.
28. • Nelson TEXTBOOK of PEDIATRICS EDITION 20
• Clinical Pediatric Tmephrology Third Edition
• Uptodate 22 version
References