Caballero B. (ed.) Encyclopaedia of Food Science, Food Technology and Nutrition. Ten-Volume Set

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and assisting the soul in crossing the river of death at

the end of life’s journey. Even the Dravidian agricul-

tural civilization recognized the practical value of

cattle to provide manure as a fertilizer or to work

pulling ploughs, apart from providing milk and its

products which had great nutritional value to families

and communities.

0017 The taboo of killing living creatures at large is tied

to the concept of ahimsa or nonviolence that prevails

widely in Hinduism, Buddhism, and Jainism. Vegetar-

ianism is practiced by devout Hindus (especially

Brahmin priests of the highest caste), Buddhists, and

Jains. It is difficult to assess the nutritional effects of

this habitual religious prescription of vegetarianism

in populations which are primarily vegetarians due to

a lack of adequate control omnivorous groups from

the same population. Nonvegetarian groups living

in the same environment may come from differing

religious or socioeconomic backgrounds. Further,

nutritional deficiencies common in developing coun-

tries where vegetarianism is practiced (for example,

India) may occur due to multiple environmental and

other factors, which makes it hard to study the

solitary effects of a vegetarian diet. However, there

is a significant amount of literature gathered over the

past few decades of the effects of vegetarianism

as practiced among Hindus, Buddhists, and other

Asian groups who have emigrated to Europe or

North America. The diet and nutritional status of

these populations has been compared with that of

omnivores of indigenous origin living in the same

environment and with similar socioeconomic back-

grounds.

Hindu Vegetarianism and Nutritional Status

0018 The nutritional adequacy of vegetarian diets (pre-

dominantly lactovegetarian) adhered to by certain

religious groups has focused on minerals such as

iron, zinc, copper, and vitamins B

and D. The ob-

servation that infants born to predominantly vegetar-

ian Hindu women have consistently low birth weight,

although birth length is comparable to those of the

indigenous Caucasian populations, has resulted in

studies to examine whether nutritional deficiency,

either of total calories or specific micronutrients

such as zinc or iron might be a factor, although gen-

etic differences cannot be completely ruled out. Zinc

and copper intakes of vegetarian, pregnant Hindu

women are lower compared to those of European

pregnant women. However, no association is found

between measures of zinc or copper status and birth

weight. Moreover, plasma zinc and copper concen-

trations are surprisingly similar in both vegetarian

and nonvegetarian Asians, whether living in India or

Europe, suggesting that vegetarianism per se may not

be associated with poor intrauterine growth and that

ethnic differences are likely to explain the detrimental

birth weight among Asians.

0019Influence of maternal vegetarianism on essential

fatty acid status of newborn and pregnancy outcome

has also been examined in Asian vegetarians com-

pared with white omnivores. Although intake of eico-

sapantaenoic acid and docosahexanoic (DHA) acid

are absent in the diets of vegetarians and infants of

these women have significantly lower DHA in their

plasma or cord blood, these factors are, again, not

related to the outcome of pregnancy such as birth

weight, length, and head circumference of infants.

The prevalence of iron-deficiency anemia is higher

among emigrant females and male vegetarian popu-

lations than that observed in omnivorous Caucasian

populations in North America and western Europe,

which may be related to the high fiber and phytate

content of the former’s diets. The major source of

cereal grains in these populations is unleavened

bread (chapatti). Although total iron intake is similar

in both groups, the nonheme form is the major source

of iron among vegetarians.

0020Diets of vegetarian Gujaratis (from the state of

Gujarat in India) living in the UK have also been

found to be lower in vitamins D and B

, although

intakes of other vitamins, such as A, B

, and folic

acid, are similar to those of the European nonvegetar-

ian controls. It is interesting that subclinical vitamin

D deficiency among vegetarian Asians (mostly Guja-

rati) in the UK resolves spontaneously during the

summer months. No such seasonal variation is found

among the Caucasian population, consistent with

their adequate vitamin D status. Increased exposure

to sunlight during the summer months followed by

cold dark winter months in a population with dietary

insufficiency of vitamin D may be an explanation for

this seasonal phenomenon. Osteomalacia and rickets

are more likely to occur in Asians living in the UK,

especially the vegetarian Hindus, and young Asian

children also have lower serum 25-hydroxycholcalci-

ferol concentrations compared to white children.

0021Risk of tuberculosis (TB) in immigrant Asians (es-

pecially Gujaratis) is also found to be high and con-

sistently higher than that recorded in their country of

origin. TB rates are three to five times higher among

vegetarian Asians than either nonvegetarian Muslims

or Asians consuming a mixed diet. A range of socio-

economic, migration, and lifestyle variables fail to

explain the risk of TB, suggesting a contributory

role of dietary factors in determining susceptibility

to disease. Vitamin D deficiency has previously been

linked to impaired host defense against TB by in-

creased mycobacterial reactivation. An early summer

peak in notified cases of TB in the UK among Asians

4936 RELIGIOUS CUSTOMS AND NUTRITION

is indicative of low postwinter trough concentration

of 25-hydroxycholecalciferol contributing to the re-

activation of latent infection.

0022 The other deficiency frequently found among vege-

tarian Hindus residing in Europe is that of vitamin

. Milk is a source of vitamin B

, but boiling milk

to extract the fat, which is a common practice among

Indians, can destroy much of the vitamin. Apparently

healthy lactovegetarian Indians tend to have lower

concentrations of vitamin B

in serum and urine

compared to nonvegetarians. This deficiency is not,

in most instances, due to a metabolic defective ab-

sorption caused by the lack of intrinsic factor which

results in pernicious anemia, but due to nutritional

cobalamin deficiency. Although vitamin B

defi-

ciency is common on the Indian subcontinent, the

evidence of a large-scale problem of megaloblastic

anemia became apparent through studies of vegetar-

ians who emigrated on a large scale from East Africa

to UK. In India, however, many cases described as

nutritional megaloblastic anemia may be due to both

cobalamin and folate deficiencies.

Seventh Day Adventists and

Vegetarianism

0023 Not all the effects of vegetarian diets prescribed by

certain religions have negative nutritional effects. In

fact, when availability and diversity of food are not

found to be confounding factors, the beneficial effects

of a vegetarian diet have been well demonstrated. A

good example is that of the most widely studied of

modern religious groups, the Seventh Day Adventist

(SDA) Christians who espouse primarily lactoovove-

getarian diets and refrain from smoking or drinking.

While these proscriptions are not found in the Bible,

the SDAs maintain that the dietary practices are based

on the general theological consideration that the

human body is the temple of the Holy Spirit and

should be protected. Numerous studies have docu-

mented the improved benefit of the SDA dietary and

lifestyle factors on their health and survival. Rates

of cancer and cardiovascular disease mortality are

much lower among Adventists from the USA, Austra-

lia, and the Netherlands compared to non-Adventist

groups. Because most SDAs do not smoke or drink

alcohol, and have varying degrees of meat consump-

tion, it is hard to distinguish between the beneficial

effects of vegetarian diets versus lifestyle factors.

However, there is evidence to suggest that among

SDAs, vegetarians are healthier than nonvegetarians

but this may not be ascribed only to absence of meat

intake.

0024 All-cause mortality among SDAs is shown to be

negatively associated with green salad consumption

and positively associated with consumption of eggs

and meat. Low meat and saturated fat intake and

high intakes of carbohydrates and dietary fiber may

be associated with these marked protective effects.

Low levels of cholesterol and blood pressure have

been observed among some SDA groups. The protect-

ive effect against major sites of cancer may be due to

higher intakes of foods providing vitamins A and C or

in some SDA groups the lower frequency of digestive

tract cancers may be due to consumption of broiled -

meat or fish, which produces little or no benzo(a)pyr-

ene and nitrosamines, which are carcinogenic prod-

ucts of heated or burnt meat. Higher consumption of

all or dried fruits has been associated with reduced

risks of lung, prostate, and pancreatic cancer among

the Adventists adjusted for sex, age, and cigarette

smoking history.

0025Although there might be some concern regarding

inadequate intakes of certain trace minerals obtained

through a vegetarian diet, dietary intakes and status

of various nutrients such as iron and zinc have been

found to be adequate among SDAs, despite the high

content of total dietary fiber and phytate of a vegetar-

ian diet and low intakes of iron and zinc from flesh

foods. Body mass index, vitamin A, and hemoglobin

concentrations among vegetarian and nonvegetarian

SDAs are generally similar, although instances of low

vitamin B

have been reported in countries where

food fortification with vitamins is not done and sup-

plementary vitamins are not consumed.

Buddhist Vegetarianism

0026Similar beneficial effects of a vegetarian diet have

been observed among young modern Chinese Bud-

dhists. Their diet is high in carbohydrates with a

moderate fat content since rice and soybean provide

most of their calorie and protein requirements. The

blood concentrations of cholesterol, glucose, and uric

acid concentration of a vegetarian Buddhist are lower,

and that of apo A-1 to apo B ratio higher, compared

to Chinese omnivores, suggesting a protective effect

of a vegetarian diet for chronic degenerative diseases.

Similarly, the blood pressure of Buddhist vegetarians

is significantly lower than those of nonvegetarians of

similar age, sex, and body mass. This might explain in

part the lower all-cause mortality observed among

Zen Buddhist priests who consume a traditional Jap-

anese diet comprising vegetables and seafood with

low amounts of meat.

Jewish Dietary Laws and Nutrition

0027Although many accounts of Jewish dietary laws,

their origins, and scientific rationalizations are found

RELIGIOUS CUSTOMS AND NUTRITION 4937

in the literature, the effects of Jewish dietary pre-

scriptions and proscriptions on the nutritional status

of Jewish people are not well-examined. The Jewish

dietary laws, called the Kashruth, are codified in

the Torah in the books of Deuteronomy 14 and

Leviticus 11. The Kashruth pertains to the type of

foods allowed for consumption and the methods of

their preparation. All fruits and vegetables and

herbivorous, ruminant animals (domesticated and

wild) whose hooves are wholly cloven are categor-

ized as ‘clean’ and permitted. Pork is forbidden

and only aquatic creatures that have at least one

fin and scale are permissible. Animals are to be

slaughtered by bleeding them to death after cutting

through the neck below the larynx (the ritual slaugh-

ter is called shehitah). Also, animals with certain

defects or injuries are not permitted. Only animals

treated thus are considered kosher. Consumption of

blood is disallowed, as is consumption of certain

portions of ‘clean’ animals such as the sciatic

nerve and certain fat portions. Carrion meat is also

forbidden and it is prohibited to cook or eat meat

and milk together. Thus, the dietary laws are com-

plex but whether their practice poses any adverse or

beneficial effects on the nutritional status of the

Jewish people who follow them is unclear. There is

no evidence to show that lack of pork meat in the diet

results in any adverse nutritional outcome. Among

the ultraorthodox Hasidic Jews living in Montreal

who are strict followers of the Kashruth, all-cause

mortality is low, primarily due to a strikingly lower

mortality from diseases of the circulatory system,

although community cohesiveness and affiliation

may, to some degree, mediate these beneficial effects.

Dietary intakes of Hasidic Jews are lower in energy,

fat, and saturated fat compared to those of other

Montrealers, Canadians, and to the NHANES II

sample, although intake of cholesterol is higher in

the Hasidics. Orthodox Jewish men and women

living in Jerusalem also have a significantly lower

consumption of total and saturated fats and higher

carbohydrates compared to secular Jews. These diet-

ary differences are reflected in the lower concen-

trations of plasma cholesterol, triglycerides, and

LDL-C concentrations observed in the former

group. A substantially higher risk of myocardial in-

farction among secular versus orthodox Jews is also

observed.

Conclusion

0028Religious customs pertaining to diet can have poten-

tially significant effects on the health and nutritional

well-being of individuals depending on the degree to

which they are prescribed. There remains a paucity of

scientific data on the effects of dietary habits of

religious origin on the nutritional status of popula-

tions, unconfounded by other cultural, social, and

economic influences. There appear to be changes in

aspects of nutritional status associated with chronic

long-term or periodic shorter-term dietary practices,

although the long-term implications of the latter

changes on health are unclear.

See also: Bioavailability of Nutrients; Coronary Heart

Disease: Etiology and Risk Factor; Iron: Properties and

Determination; Minerals – Dietary Importance;

Vegetarian Diets; Yogurt: Yogurt-based Products

Further Reading

Dwyer JT (1988) Health aspects of vegetarian diets. Ameri-

can Journal of Clinical Nutrition 48: 712–738.

Glanz K and Kolonel LN (1998) Culture, religion, diet

and health: challenges and opportunities. Nutrition 14:

238–239.

Grivetti LE and Pangborn RM (1974) Origin of selected

Old Testament dietary prohibitions. Journal of the

American Dietary Association 65: 634–638.

James EO (1979) Cultural and religious taboos related to

food. Progress of Food Nutrition Science 3: 67–77.

Jiggets JI (1949) Religion, Diet, and Health of Jews. New

York: Bloch.

Johnston PK and Sabate J (1999) Third International Con-

gress on Vegetarian Nutrition. Proceedings of a sympo-

sium held in Loma Linda, CA March 24–26, 1997.

American Journal of Clinical Nutrition 70: 3(S).

Rashed A (1992) The fast of Ramadan. British Medical

Journal 304: 521–522.

Journal of the American Dietary Association 62:

253–261.

Robson JRK (1980) Food, Ecology and Culture. Readings

in the Anthropology of Dietary Practices. New York:

Gordon and Breach.

Sakr AH (1975) Fasting in Islam. Journal of the American

Dietary Association 67: 17–21.

Shatenstein B and Ghadirian P (1998) Influences on diet,

health behaviours and their outcome in select ethnocul-

tural and religious groups. Nutrition 14: 223–230.

4938 RELIGIOUS CUSTOMS AND NUTRITION

RENAL FUNCTION AND DISORDERS

Contents

Kidney: Structure and Function

Nutritional Management of Renal Disorders

Kidney: Structure and Function

T T Rosa, University of Brasilia, Brasilia, Brazil

Background

0001 The human kidneys are located in the lumbar area, as

a pair in the retroperitoneal space, and are composed

of about a million nephrons, which are the functional

units. Each nephron contains a glomerulus which

carries out blood filtration and there is tubular

system, divided into 14 segments, which are different

morphologically and functionally. The combined

action of these structures produces urine. The glom-

erulus is located in the outer part of the kidneys,

called the cortex, and the tubules are located in the

inner part, called the medulla. These structures are

connected by interstitial tissue and contained by a

fibrous capsule, named Bowman’s capsule, in a

similar shape to a bean (Figure 1).

0002 Within the kidney are located the renal hilum,

as well as the renal pelvis, formed by the exit of the

renal vein, which it drains from the vena cava;

the renal artery, a branch of the abdominal aorta

artery; the lymphatics; and a nerve plexus. In addition

to these components are those of the urinary

branches. These are the renal pelvis and ureter,

which transports urine to the bladder, from where it

exits via the urethra, completing the system of renal

excretion (Figure 2).

Glomerular Ultrafiltration

0003The first stage of the process of urine formation is

glomerular ultrafiltration. About 170 l of plasma is

ultrafiltered every 24 h, representing more than 30

times volume. The resulting product, in the form of

urine, corresponds to less than 1% of that volume.

The difference is the result of the balance between

the reabsorption process and the secretion process

accomplished by the tubular system.

0004Marcello Malpighi first described the structure

which is now called the glomerulus in 1662. As a

result, the corpuscle was just known as corpuscles

of Malpighi for a long time. Carl Ludwig, in the

Renal convexity

Renal vein

Renal artery

Renal pelvis

fig0001 Figure 1 Macroscopic renal structure.

Column of bertin

Medullary pyramid

Calyx

Pelvis

Cortex

Medullary boundary

fig0002Figure 2 Renal hilum.

RENAL FUNCTION AND DISORDERS/Kidney: Structure and Function 4939

nineteenth century, described the ultrafiltration pro-

cess as the passage of water, electrolytes, and small

molecules, from the glomerular capillaries to Bow-

man’s space. In 1924, this theory was proven: glu-

cose, chloride, but no proteins were detected in the

Bowman’s space. All the energy for that process is

created by the heart, acting at the level of the renal

microcirculation, and this characterizes ultrafiltra-

tion as a physical phenomenon.

0005 Glomerular filtration rate (GFR) in humans is

approximately 120 ml min

1

. It is the result of ultra-

filtration achieved by about 2 million nephrons.

0006 As a physical phenomenon ultrafiltration results

from a balance of pressure between the glomerular

capillary and the internal space of Bowman’s capsule.

The glomerular tuft forms a conductive system in

parallel, located between the afferent and the efferent

arterioles (Figure 3). The pressures involved in this

process are as follows:

P

¼ P

IG :

ð1Þ

where P

represents the variation in hydrostatic

pressure resulting from the difference between P

the hydrostatic intraglomerular pressure, and P

pressure inside the Bowman’s capsule. It is similar to

the physical principle behind a domestic water filter.

000 7 The concentration of proteins in the plasma also

interferes with the process, as it adds to the filtrate a

pressure that is opposed to the hydrostatic pressure,

called oncotic pressure (P

). That pressure represents

a vector that addresses the filtered flow in an inverse

direction, in other words, from Bowman’s capsule to

the glomerular capillary once the protein concentra-

tion is minimum in the Bowman’s capsule, close to

zero, because the wall of the glomerular capillary

does not allow proteins to pass. In that way, the

effective filtration pressure (P

) is expressed in agree-

ment with eqns (2) and (3):

¼ðP

ÞP

ð2Þ

¼P

P

:ð3Þ

0008The renal plasma flow should be adapted to allow a

balance of those pressure forces and the permeability

of the glomerular wall should be unaffected if the

process is to happen in a physiologic way. This last

variable is represented by a variable called the coeffi-

cient of hydraulic conductance and represented by the

symbol K

. In comparison to the domestic filter, this

coefficient measures the porosity of the filter. In the

glomerulus it is defined by the product of the intrinsic

permeability of the glomerular wall (K) for the total

surface available for the filtration process (S), and is

represented as follows:

¼ K  S:ð4Þ

0009The decrease in K

determines a decrease in GFR,

that it is not as pronounced as variations due to

alterations in hydraulic and oncotic pressure.

0010To tune so many variables involved in glome-

rular ultrafiltration it is necessary for there to be

self-regulation, so that variations in systemic blood

pressure (SBP) do not interfere markedly in the pro-

cess of urine formation that begins with ultrafiltra-

tion. If such a mechanism did not exist, dynamic

variations in SBP would affect GFR.

0011Self-regulation is effected by an increase or de-

crease in resistance of the afferent and efferent arteri-

oles defined by vasoconstriction or vasodilatation of

these arterioles, if SBP falls or rises, respectively. This

vascular movement is caused by three factors: vaso-

motor reflex, when the vein contracts its smooth

muscle and reduces its diameter, when there is an

increase in hydrostatic pressure within; metabolite

production in response to the increase in blood flow

in those arterioles, causing vasoconstriction; and the

mechanism of glomerular tubule feedback.

0012In this last factor, the tubular structure is involved;

this is called the macula densa and is located in

the distal convoluted tubule. Alterations in the load

of filtered sodium give rise to renin secretion; renin

is produced in the cytoplasm of differentiated cells,

and is present in the macula densa and in cells

contiguous to the glomerulus, which comprise the

justaglomerular device. Production of increased renin

results in an increase in circulation of angiotensin II

level, by a cascade of reactions shown in Figure 4.

Angiotensin II stimulates local receptors in the afferent

PH (15)

PO (25)

PH (15)

PO (30)

PH (15)

Afferent

arteriole

mmHg

Efferent

arteriole

PH (50)

PO (20)

fig0003 Figure 3 Renal microcirculation.

4940 RENAL FUNCTION AND DISORDERS/Kidney: Structure and Function

arterioles promoting vasoconstriction and a decrease

in flow in the nephrons and a consequent decrease in

glomerular filtration rate, balancing out the process

of glomerular filtration associated with the secretion

and tubular reabsorption, and resulting in the glom-

erular tubular balance.

0013 To estimate GFR it is necessary to carry out clear-

ance of a substance that is only filtered, and is not

reabsorbed or secreted by tubules. Clinically, it is

preferred for a substance to be produced endogen-

ously, rather than having to administer an exogenous

drug. Calculation of the endogenous creatinine clear-

ance is commonly used. The clearance of any sub-

stance is always given by the product of its urinary

concentration (U) and urinary flow (V), divided by its

plasma concentration (P). Urinary flow is always

calculated in ml min

1

0014 In fact creatinine is not ideal for calculation of

GFR, as it is partly secreted by the renal tubules,

and appears in the urine as a result of filtration and

a small amount of secretion, but results are very close

to those obtained with inulin, an exogenous sub-

stance, which is totally filtered, and is used in experi-

mental assays for the exact determination of GFR.

Besides, the method of creatinine dosage is easy and

cheap, which is a distinct advantage in clinical use.

0015 In contrast, the simple creatinine level in plasma

gives us an idea of how renal filtration works, because

it is always in balance in the organism, as are almost

all endogenous products. That means that its excre-

tion should equal its production. Mathematically we

have: creatinine production (Prod

) ¼urinary excre-

tion of creatinine (U

) urinary flow (V). As with

the creatinine, the excreted load is the same as the

filtered load, and can be written: Prod

¼plasma

concentration of creatinine (P

) GFR, that is:

¼Prod

GFR. As creatinine production is

constant, its plasma concentration is an inverse

hyperbolic function of GFR.

0016Most components in plasma are filtered by the

kidney.

Tubular Reabsorption

0017Unlike glomerular filtration and tubular secretion,

tubular reabsorption is not part of the process of

renal excretion. In fact it is a renal mechanism that

saves essential element, to the homeostasis of the

internal environment, such as water, glucose, and

amino acids. The transport of fluid from the inside

of the tubule to the internal environment through the

tubular wall is complex and involves several mechan-

isms. Some of these spend energy of the organism

(adenosine triphosphate or ATP), while others are

made passively, by gradients created among the com-

partments involved. Those gradients may be physical

(differences in the electric charge or in the pH),

chemical (differences in the concentrations of several

substances) or osmotic (difference of concentration of

solutes). There is also so-called facilitated transport,

such as when glucose transport is facilitated by

sodium transport. Those substances that need carriers

are located in the membrane of the tubular cells

which are linked to the substance to be transported

in the border with the inner tubule. The carriers make

transport through the cytoplasm to the border with

the renal interstice, where the peritubular capillaries

are located, liberating them to the internal environ-

ment of the organism.

0018Of the 170 l plasma that is filtered, and one more

small rate of secretion, tubular reabsorption is about

1.5–2 l day

1

to the external environment, in the form

of urine. The difference is returned to the internal

environment by tubular reabsorption.

0019The main site responsible for reabsorption is the

convoluted proximal tubule, which is the tubular

portion that is located immediately after the glomeru-

lus. These cells have quite a heterogeneous form and

the borders contain microvilli that provide a larger

contact surface with the fluid to be reabsorbed, opti-

mizing the process. Despite this, reabsorption, as well

as secretion, takes place along the whole renal tubular

system.

0020The main substances reabsorbed in the renal

tubules are amino acids, glucose, electrolytes, bicar-

bonate, and urea.

ANGIOTENSINOGEN

ANGIOTENSIN I

ANGIOTENSIN II

ANGIOTENSIN CONVERTING ENZYME

RENIN

fig0004 Figure 4 The renin–angiotensin system.

RENAL FUNCTION AND DISORDERS/Kidney: Structure and Function 4941

Tubular Secretion

0021 Tubular secretion is the term given to the transport of

substances from the medullary peritubular capillary

to the inside of the tubule. It happens predominantly

in the final part, the straight section, of the proximal

convoluted tubule. It is also a method of renal excre-

tion and can be calculated by the clearance of sub-

stances that are not filtered, or reabsorbed, but which

appear in the urine, such as paraaminohippurate.

This is a salt of paraaminohippuric acid and it is

used to calculate renal plasma flow, after excretion.

The transport mechanisms involved in secretion are

very similar to reabsorption, especially as regards

energy (ATP) expenditure.

0022 The main substances secreted by the kidneys are

urea, hydrogen, organic acids, and exogenous sub-

stance such as drugs and antibiotics.

Renal Metabolism of Water

0023 Water makes up the largest part of the human organ-

ism, comprising about 80% of the total. The sensation

of thirst originates in the hypothalamic center of thirst,

which is sensitive to a variation in plasmatic osmolal-

ity of at least 1% and it is located in paraventricular

and supraoptical nuclei. An increase in plasmatic

osmolality stimulates the secretion of antidiuretic hor-

mone (ADH) from the hypophysis as a result of those

hypothalamic impulses. ADH acts, among other struc-

tures, at the level of the collector ducts, in the distal

nephron, promoting the reabsorption of water and the

consequent normalization of plasma osmolality.

0024 In this way, the final urine under the action of ADH

is more concentrated, it has larger osmolality. When

there is an excess of water in the organism, an inverse

mechanism results; there is inhibition of ADH and the

urine produced has less osmolality. The first situation

is more frequent, when maximum capacity of urinary

concentration is reached, whose resultant osmolality

can be up to 1200 mosm ol l

1

0025 The mechanism by which nephrons concentrate

urine is called countercurrent mechanism (similar to

that described by thermodynamics) and it involves

the proximal segments, the loop of Henle, and the

distal segments of the renal tubules. It acts by an

established osmolar gradient in the renal medulla

and in inside the tuble, as a result of active transport

of NaCl and the diffusion of H

O through mem-

branes with special permeabilities along the long

loop nephrons, which are especially adapted for that

function, located in the boundary between cortex and

medulla. The result of that complex mechanism is a

concentration of urine in such a way that the plasma

osmolality is maintained constant and normal.

Endocrine Functions of the Kidneys

0026One of the most important hormones produced by

the kidney is 1a-25-dihydroxycholicalciferol, the

active form of vitamin D

, and it acts directly in

the renal metabolism of calcium and of phosphorus.

A fall in plasma calcium stimulates the secretion of

parathormone (PTH) in the parathyroid glands and

so, they act in the renal medulla, promoting the syn-

thesis of activated vitamin D

. This acts in the small

intestine, increasing the reabsorption of calcium in

the bone tissue, increasing demineralization, and in

the renal tubules, increasing reabsorption, at the same

time as it promotes an increased excretion of phos-

phate, as phosphaturia.

0027A reduction in phosphate in the plasma stimulates

vitamin production, directly activated by vitamin D

by the renal medulla and, in the absence of PTH renal

tubular reabsorption of phosphate and greater excre-

tion of calcium (calciuria) are promoted.

0028Thus the product of plasma concentration between

calcium and phosphorus is maintained constant.

Action of Kidneys in the Acid–Base

Balance

0029In addition to the important mechanism of acid–base

control accomplished by the lungs, promoting the

elimination of the carbon gas in its volatile form, the

kidneys also participate in controlling the metabolism

of bicarbonate (HCO

) and of the ion H

, which are

respectively reabsorbed and secreted by the renal

tubules.

0030This balance is fundamental to maintain organic

biochemical reactions that keep constant blood pH,

at around 7.4.

0031The transport of those two ions takes place in the

proximal convoluted tubule and in the convoluted

distal tubule. It happens in a connected way: one ion

secreted for each reabsorbed HCO

molecule. In

the proximal convoluted tubule, bicarbonate is

regenerated from the inner tubule by two principal

mechanisms: excretion of carbonic acid dissolved in

the tubular fluid and secretion of fixed acids, such as

sulfuric, hydrochloric, and phosphoric, among

others. At the level of the distal convoluted tubule,

there is reabsorption of HCO

starting from the

cellular synthesis of ammonia with the secretion of

the ammonium ion.

Renal Control of Blood Pressure

0032In the distal convoluted tubule is located the macula

densa: it has longer cells and cytoplasmic granules.

Close to it there are segments of afferent and efferent

arterioles that have a greater amount of cytoplasmic

4942 RENAL FUNCTION AND DISORDERS/Kidney: Structure and Function

granules. These granules correspond to renin, the

proteolytic enzyme that is synthesized there. This

group of structures is termed the juxtaglomerular

apparatus.

0033 The main incentives for renin production are a

reduction in blood pressure with a consequent fall in

hydrostatic pressure of the afferent arteriole, and a

reduction in renal plasma flow and variations in the

concentration of sodium in the distal convoluted

tubule.

0034 Renin acts on a substratum called angiotensinogen,

a duodecapeptide, of hepatic synthesis, transforming

it to the decapeptide called angiotensin I. This under-

goes action by another proteolytic enzyme, called

angiotensin-converting enzyme (ACE), which is

mainly synthesized in the capillary endothelium, cre-

ating the octapeptide angiotensin II, which is a sub-

stance which has a larger effect on the vasoconstrictor

produced by the organism.

0035 Receivers exist for angiotensin II in the afferent and

efferent arterioles, altering GFR, when there is an

increase in that peptide in the circulation. In the

systemic circulation there is an increase in peripheral

resistance and therefore also in blood pressure. There

are also receivers in the adrenal cortex which when

stimulated synthesize aldosterone, a hormone whose

main action is to promote reabsorption of sodium in

the distal convoluted tubule.

0036 Thus it is easy to understand that arterial blood

pressure is controlled by this renal mechanism

and dysfunction of is system, called the renin–

angiotensin–aldosterone system, will result in arterial

hypertension.

0037 In short, the renal structure is adapted to achieve

vital functions for the human organism. The most

difficult stage in the evolution of animal life on

earth was considered to be the adaptation from an

aqueous environment, the kidneys are essential to

make life on earth viable, saving water and mineral

salts and maintaining the necessary metabolic homeo-

stasis for the hemodynamic adaptation and of the pH

of blood.

See also: Electrolytes: Analysis; Water–Electrolyte

Balance; Acid–Base Balance; Renal Function and

Disorders: Nutritional Management of Renal Disorders;

Water: Physiology

Further Reading

Goldman L (2000) Cecil Textbook of Medicine 21st edn.

Philadelphia: WB Saunders.

Levine SA (ed.) (2000) Brenner & Rector’s The Kidney, 6th

edn. Philadelphia: WB Saunders & Co.

Miller RD (2000) Anesthesia, 5th edn. Philadelphia:

Churchill Livingstone.

Nutritional Management of

Renal Disorders

B E Engel, Royal Infirmary, Stoke-on-Trent, UK

Introduction

0001The nutritional state of the body is dependent on the

intake of adequate amounts of nutrients in food and

fluids and the ability of the body to utilize these

substances and dispose of the excess and the waste

products created from metabolic processes. One of

the main functions of the kidney is the disposal

of some of these waste products, in particular, the

nitrogenous waste from the breakdown of protein as

well as excretion of fluid, sodium, potassium, phos-

phate, hydrogen ions, and organic acids, in order to

achieve homeostasis. The kidney also has a synthetic

function converting 25-hydrocholecalciferol to 1,25-

dihydroxycholecalciferol (1,25(OH)

D – the active

form of vitamin D), and in producing the hormone

erythropoietin (EPO), which is important in promot-

ing the formation of red blood cells. In many types of

kidney disease, these functions are impaired, resulting

in the accumulation of toxic waste products in the

blood, and the development of hypertension, bone

disease, anemia, and hyperlipidemia.

0002The main aims of dietary management in kidney

disease are therefore to:

0003Reduce the accumulation of waste products and

thus prevent or ameliorate uremic toxicity and the

adverse effects of alterations in various metabolic

pathways.

0004Maintain or improve nutritional status (identify-

ing and treating malnutrition at an early stage).

0005Maintain or improve the kidney patient’s quality

of life.

Finally, dietary interventions may help contribute to

slowing down the progression of the disease.

0006The various kidney diseases that lead to end-stage

renal failure (ESRF) show many similarities in their

clinical and pathological features, and thus dietary

management is not necessarily modified by the ori-

ginal cause of the disease. In this chapter, the main

subjects discussed are: (1) chronic renal failure, (2)

nephrotic syndrome, (3) ESRF requiring dialysis and

transplantation, (4) acute renal failure, and (5) renal

stone disease.

Chronic renal failure (CRF)

0007Giovanetti described CRF as a chronic reduction of

glomerular filtration rate (GFR) below the normal

RENAL FUNCTION AND DISORDERS/Nutritional Management of Renal Disorders 4943

range (c. 120 ml min

1

) irrespective of the underlying

cause (Table 1). The increase in plasma constituents

such as creatinine and urea is used as a general marker

to indicate the severity of the disease (Table 2).

Reciprocal plots of creatinine against time are com-

monly used to chart the progression of CRF. The

excretion of creatinine (formed from creatine and

phosphocreatine in muscle tissue) occurs predomin-

antly by renal filtration. A decrease in GFR below

50% of normal leads to a rise in plasma creatinine.

However, as creatinine production is proportional to

lean body mass and is also influenced by animal

protein intake, a loss of lean body mass or decreasing

appetite during the course of CRF can give the false

impression that the rate of decline of renal function is

slowing down. In addition, a plasma creatinine of

1000 mmol l

1

may indicate a GFR of < 10 ml min

1

in a 70-kg man, whereas a creatinine of 600 mmol l

1

would indicate the equivalent level of renal function

in a person of lower body weight.

Protein Metabolism and Requirements

0008 A well-planned and monitored reduction in protein

intake in CRF patients will decrease the amount of

nitrogenous waste, phosphorus, potassium, and acids

that must be dealt with by the kidney. Urea is the

main metabolite of protein, and in CRF, plasma urea

increases as GFR decreases. A decrease in the urea:-

creatinine ratio after starting a reduced protein diet

may be used as a measure of compliance with the diet.

Other factors, however, may raise plasma urea fur-

ther, e.g., a high dietary protein intake, drugs such

as frusemide and steroids, gastrointestinal bleeding,

and a hypercatabolic state leading to muscle catabol-

ism. Urea itself is nontoxic, but its elevation correl-

ates with the rise in plasma levels of more toxic

compounds, e.g., guanidines, amines, phenols, and

organic acids. Plasma urea levels are therefore used

as a surrogate marker for these toxins.

0009Most of the research in this area has focused on the

effect of a low-protein diet on slowing down the

progression of renal disease. The diets have aimed to

provide 0.6 g of protein per kilogram of ideal body

weight (IBW), which is the minimum requirement

advised by the World Health Organization. It is still

recommended that at least 50% of the protein should

be of high biological value (HBV) – essentially from

meat, fish, and diary products in order to provide all

essential amino acids, although vegan and vegetarian

diets can maintain the nitrogen balance as long as

proteins are obtained from a combination of low

biological value (LBV) sources, such as grains, pulses,

etc. The protein intake from food can be reduced

further to 0.3 g kg

1

IBW if the diet is virtually vege-

tarian and supplemented with essential amino acids

or their keto analogs. In practice, even with consider-

able support from dietitians, it seems difficult – cer-

tainly in Western society – to maintain this level of

protein restriction. In the largest trial ever completed

on this subject, the Modification of Diet in Renal

Disease, patients’ actual intake was 0.7–0.8 g protein

per kilogram per day. At this level, overall nutritional

status was maintained throughout the 2 years of the

trial, although the energy intake was less than the

recommended 35 calories per kilogram per day. A

reduction of protein intake by 0.2 g kg

1

resulted in

a 30% reduction in the rate of decline of GFR, i.e., a

prolongation of the time to ESRF by 41% in patients

with advanced renal failure. Some clinicians argue

that this level of improvement is not significant

enough to justify a diet that is difficult to achieve,

requires a lot of support from dietitians as well as

family, and may lead to nutrient deficiencies in the

long term. There are none the less other benefits from

reducing protein intake: the improved biochemical

indices that result from this intervention will help

reduce some of the classic symptoms of uremia that

are related to the accumulation of protein metabolites

and imbalances particularly in phosphorus, potas-

sium and lipid metabolism (Table 3).

Energy Requirements

0010There is no evidence to suggest that requirements are

affected by renal disease itself. Calculation of energy

requirements should be made depending upon the

need for weight loss, maintenance, or gain in the

normal way, e.g., Schofield or Harris–Benedict equa-

tions or 30–35 kcal kg

1

IBW. As hyperlipidemia

(increased triglycerides and/or cholesterol) and some

degree of glucose intolerance are common, the source

of calories should be from complex carbohydrates

tbl0001 Table 1 Main causes of chronic renal failure

Glomerulonephritis Hypertension

Chronic pyelonephritis Polycystic kidney disease

Obstructive, reflux, analgesic

nephropathies

Systemic disease: scleroderma,

systemic lupus erythematosus

Diabetic nephropathy Vasculitis

Renal transplant failure Myeloma, amyloidosis

tbl0002 Table 2 Stage of renal failure related to creatinine level

Stage Plasma creatinine

concentration (mmoll

1

)

Glomerular

filtration rate

(mlmin

1

)

Early 120–150 40–60

Moderate 150–300 20–40

Advanced >400 10–20

End-stage renal failure >600 – requires RRT <10

4944 RENAL FUNCTION AND DISORDERS/Nutritional Management of Renal Disorders

and mono-polyunsaturated fats (with overall fat

intake providing 30% of the energy) in line with

advice for healthy eating.

Vitamins and Minerals

0011 Some of the clinical features of uremia may be linked

to subclinical vitamin and mineral deficiencies. Diet-

ary protein, phosphate, and potassium restrictions

will limit the intake of various micronutrients, and

even when intake is adequate, the metabolic path-

ways may be affected, reducing the availability or

efficacy of the nutrients. Specifically, a low-protein

diet was found to contain low levels of B vitamins (B

), iron, calcium, and zinc. A low-potassium

diet will limit folic acid and vitamin C intake. How-

ever, there may be reduced renal losses of some nutri-

ents, and cases of hypervitaminosis A have been

recorded. It is recommended that vitamin and mineral

status should be part of a renal patients regular

nutritional assessment.

Phosphorus and Calcium

0012 Hyperphosphatemia and hypocalcemia are character-

istic of CRF. A decreasing GFR will lead to a reduced

renal clearance of phosphate, even at the moderate

stage of CRF, and eventually will lead to an increased

plasma phosphate. Simultaneously low levels of

active vitamin D cause a reduction of calcium absorp-

tion from the gut, hence lowering the plasma calcium.

These two factors stimulate parathyroid hormone

(PTH) release, which in turn causes bone resorption.

The release of calcium from the bone is an attempt

to normalize plasma calcium levels, unfortunately at

the expense of the integrity of the skeletal system (and

a further rise in plasma phosphate), resulting in osteo-

dystrophy. A raised plasma calcium phosphate

product (> 5 mmol

) also results in calcification of

soft tissues and has been linked with an increased

risk of cerebrovascular disease (stroke) in these

patients.

0013A low-phosphorus diet (c. 0.3–0.5 mmol per kilo-

gram IBW per day) (Table 4), in combination with

phosphate binders such as calcium carbonate, has

been prescribed to maintain plasma phosphate within

the normal range. A phosphorus intake at the lower

recommended level can only be achieved with some

degree of protein restriction, particularly the HBV

proteins. This diet will also limit calcium intake,

hence there is a dual role for calcium tablets: as a

binder of phosphorus and to provide a calcium sup-

plement. Prescription of 1,25-dihydroxy or 1-hydroxy

cholecalciferol can help to suppress PTH production.

Calcium levels must be monitored regularly, as, due

to the medication, there is a risk of hypercalcemia

from increased intestinal absorption. Plasma levels

for phosphate and calcium should be maintained

within the normal ranges. As yet, there is no consen-

sus regarding the optimum level of renal failure at

which to advise a reduction in phosphorus intake, i.e.,

it may be of benefit to reduce intake before plasma

levels exceed the normal range, as PTH may already

be increasing in order to maintain homeostasis.

Potassium

0014Hyperkalemia does not tend to develop until the

GFR < 10 ml min

1

(i.e., ESRF). It can occur in mod-

erate CRF under certain circumstances such as in-

creased catabolism: infection, trauma, acidosis, or

medication: angiotensin-converting enzyme (ACE)

inhibitors, cyclosporin A, and EPO. A raised plasma

potassium > 6.5 mmol l

1

can increase the risk of

asystolic cardiac arrest. Hence, it is advised that levels

should be maintained within the normal range using a

combination of dietary restrictions of high-potassium

foods and appropriate cooking methods such as

tbl0003 Table 3 Uremic manifestations

Systemaffected Uremic symptoms

Cardiovascular High blood pressure, fluid

overload, pericarditis,

cardiomyopathy

Gastrointestinal Nausea, vomiting, gastritis

Peripheral nervous system Neuropathy, myopathy

Central nervous system Confusion, drowsiness, impaired

higher mental functions,

insomnia, coma

Blood Anemia

Skeletal Renal osteodystrophy, bone pain,

fractures

Skin Pruritis, pigmentation,

calcification

tbl0004 Table 4 Phosphate (mg):protein (g) ratio of some common foods

Phosphate:proteinratio < 10 Beef, lamb, turkey, chicken, pork, cod, haddock, tuna, cornedbeef

Phosphate:protein ratio 10^15 Bacon, ham, meat paste, plaice, plaice, herring, mackerel, salmon, cottage cheese, whitebread, whitepasta

Phosphate:protein ratio 15^20 Liver, pilchards, mussels, prawns, soyamilk, peanuts, pulses, white rice

Phosphate:protein ratio > 20 Milk, icecream, cheese, yogurt, pate, roe, sardines, whitebait, nuts, chocolate, wholemealbread, brownrice,

brown pasta, bran flakes, sponge, scones

NB: Although wholemeal products are higher in phosphate, patients are still encouraged to have them as part of a healthy diet and to help bowel function.

RENAL FUNCTION AND DISORDERS/Nutritional Management of Renal Disorders 4945