Chronic Renal Failure
A Homeopathic approach
Dr.Satheesh Kumar.P.K  BHMS,MD(Hom)
Medical Officer, Dept. of Homoeopathy, Govt. of Kerala
 

“The composition of the blood and internal environment is determined not by what the mouth ingests but by what the kidney keeps”
 
Definition:
Chronic renal failure is irreversible deterioration in renal function, or if renal failure persists more than six months it is termed chronic renal failure. (Renal failure- simply due to deficiency of nephron.)

 
The kidney has the capacity to regain function following acute renal injury. Renal injury of a more prolonged nature (like SLE, DM, Hyper tension) often leads to progressive and irreversible destruction of nephron mass. Such reduction of renal mass, in turn causes structural and functional hypertrophy of surviving nephrons. The ensuing Impairment of the excretory, metabolic and endocrine function of the kidney leads to the development of the clinical syndrome of uraernia. [Uraemia is the term generally applied to the clinical syndrome that result from profound loss of renal function.]
(Endocrine function of the kidney responsible for the production of certain hormone that has local and systemic effect.

1. Renin-angiotensin system,
2. Vitmine D,
3. Erythropoetin,
4. Prostaglandin and
5. Kallikrien are some among them)
 
Etiology:
Chronic renal failure may be caused by any condition, which destroys the normal structure and function of the kidney.
Glomerulonephritis in its several forms was the most common initiating cause of CRF in the past. Diabetes mellitus and hypertensive renal disease are now the leading causes of chronic renal failure.

Aetiology of chronic renal failure can be classified as follows:
1.Congenital and inherited diseases
a) Polycystic kidney disease [infantile or adult type]
b) Alport’s syndrome – is an inherited gloirierular disease and is characterized by destructive changes in glomerular basement membrane. The glomerular basement membrane is irregular with longitudinal layering, splitting or thickening and patient develop hematuria, progressive glomerulosclerosis and renal failure. Alport’s syndrome is fatal in early life.
c) Fabry’s disease -is an inborn error of glycosphirigo lipid metabolism characterized by telangiectatic skin lesion, hypohydrosis, corneal and lenticular opacities, aeroparesthesia and vascular disease of the kidney, heart and brain
2.Vascular disease
a) Arteriosclerosis
b) Vasculitis. 
3. Glouierular disease
a) Proliferative glomerulo nephritis
b) Cresentic G.N.
c) Membranous G.N’.
d) Mesangio capillary G.N.
e) Giomerulo sclerosis 
4. Interstitial disease
a) C/C infective interstitial nephritis, [pyelo nephritis]
b) Vesico--ureteric reflux - is the pathological condition in which urine from the bladder regurgitates in to the ureter and ascends to kidney during the process of micturition. Urinary tract infection is the common complication of vesico— ureteric reflux. The initial damage occurs in the poles of the kidney and these leads to scarring.
c) Tuberculosis
d) Analgesic nephropathy
e) Nephro calcinosis – is a complication of hyper parathyroidism in which calcium become deposited in the renal tubules.
f) Schistosomiasis
g) Unknown origin.
5. Obstructive uropathy.
a) Calculus
b) Retro peritoneal fibrosis,
c) Prostatic hypertrophy,
d) Pelvic tumor,
e) Other causes – A] Organic causes that obstruct the lumen of ureter like stone, blood cloat, caseous or necrotic debris etc.
B] Functional causes like congenital neuro-muscular defect.
 
6. Systemic diseases.
a) Amyloidosis,
b) Multiple myeloma
c) Radiation nephropathy,
d) Connective tissue diseases.
 
PATHOGENESIS 
Chronic renal failure is due to progressive destruction of nephrons. As the nephrons are destroyed the parenchyma shrinks and it is replaced by fibrosis. The surviving nephrons undergo hypertrophy— this gives the appearance of a granular contracted kidney. The renal function is maintained by the hypertrophied nephrons. Since the concentrating function is impaired, adjustment of the urine volume become defective and polyurea with urine specific gravity around 1010 occurs. The blood pressure goes up and this forms of secondary hypertension exerts deleterious influence on the kidney, heart, and brain.

Hypertension causes renal damage (in addition to being produced by It) and when it is severe, renal failure progress rapidly with the patient dying of uraemia or cardio vascular system complication, after a relatively short illness. If hypertension is absent or can be readily controlled, the patient may live for years, despite severe impairment of renal function. The early phase of the disease is asymptomatic, since the kidney has considerable reserve function. Symptoms and biochemical abnormalities are evident only when the renal function has deteriorated to less than 35% of the normal.
(In CRF the tubules loss their capacity to concentrate and dilute the urine, then the specific gravity become fixed at 1010. This is called isosthenuria).
When the renal function is between 35 % and 25 % of the normal, symptoms like pallor, tiredness and nocturia are evident. Blood urea and serum creatinine are elevated. [Normal blood urea less than 40 mg/dl; creatinine— 0.4 to 1.4rng/dl] and serum bicarbonate may be decreased slightly [normal 24- 28 meq/lit]
 
Several intercurrent factors precipitate the development of advanced renal failure this patient. These are:
Dehydration and electrolyte imbalance
Infection
Excessive protein intake
Cardiac failure
Alcoholic bouts
Trauma
The use of nephrotoxic drugs
Blood loss
When the insufficiency is moderate (functions falls to 25% to 15% of normal) symptoms like fatigue, nausea, anorexia, impotence, metabolic acidosis and bone pain may develop.
When the renal function is below 15% the full-fledged uraemic syndrome develops. In this all the system are affected and clinical feature are referable to all organs. General symptoms include - fatigue, lethargy, anorexia, nausea, loss wt. headache, confusion and mental disturbances. The urine volume is may be high in the uncomplicated cases with nocturnal polyurea. Urine volume is reduced when oliguric renal failure or cardiac failure develops.
 
CLINICAL FEATURES 
In the early stages of disease, the patient may be asymptomatic and the existence of renal insufficiency may be revealed by the discovery protenuria, anaemia, hypertension or raised blood urea during routine examination. When the renal function deteriorates slowly, patient remain asymptomatic until the glomerular filtration rate is 15m1/rnt or less.

Signs and symptoms of chronic renal failure referable to almost all system. They are as follows
1.Neurological: Fatigue, insomnia, reversal of sleep rhythm, peripheral neuropathy, muscular irritability, convulsion and coma. Low calcium level leads to increased neuro muscular irritability arid can leads to tetany and to convulsion. Loss of tendon jerk and slowing of nerve conduction velocities are also present.
2.Gastro intestinal tract: Anorexia, nausea, vomiting and peptic ulcer. Nitrogenous waste product retension has an important effect on the gastrointestinal tract. Anorexia and vomiting tends to limit caloric intake leads to wasting. Constipation from reduced food intake. Some will develops ulceration at numerous points along the gastrointestinal tract with profuse bloody diarrhoea.
3.Hematological: Normochromic normocytic anaemia and bleeding tendencies due to platelet dysfunctions. A nitrogenous compound — guanidosuccinic acid contribute to platelet dysfunction. Patient with renal failure are usually uniformly anaemic even when they are maintained biochemically normal haemodialysis and when no bleeding tendency is apparent. It is thought that this anaemia is due to the lack of the hormone erythropoietin. Erythropoietin stimulate the erythropoisis. Erythropoietin is formed in the renal tissues probably due to the effect of Adrenal cortico trophic hormone.
4. Endocrine: Secondary hyperthyroidism, amenorrhea, infertility and impotence.
5. Dermatological:
Swallow pigmentation, intractable pruritus (calcium deposition in tissue especially in skin-giving rise to pruritus) excoriation and uremic frost (whitish precipitate of urea crystals on the skin occurring in advanced uremia) occur in skin. Normal urine contains a variety of pigments and has a yellowish brown appearance. In renal failure these pigments are retained in the body and imparting a bronzed appearance to the skin. Because of this bronzed appearance, most of the uraemic patients look less anaemic than they are.
6. Skeletal:
Skeletal changes include mainly renal osteodystrophy, which includes osteomalacea, osteoporosis, ostitis fibrosa or rickets. Skeletal manifestations are due to disordered calcium and phosphate metabolism.
7. Cardio vascular system:
Hypertension, cardiac failure, pericarditis, myocrdiopathy and accelerated atherosclerosis. Uraemic pericarditis was regarded as a harbinger of doom. Death was usual with in a few days of pericarditis being detected. The patient is usually complaints of left sided pleuritic pain and this pain has some postural characteristic. (For example: pain becomes less severe when the patient bends forward). Here there is a constant danger of bleeding in to the inflamed pericardial sac with cardiac temponade and sudden death. Diagnosis by X-ray and pericardial friction rub.
8. Occular:
 Red eye (due to conjuctival calcium deposition and congestion). Calcium deposition in the cornea and hypertensive retinopathy. 
9.Respiratory: Kuss maul’s respiration, uremic lung (increased pulmonary capillary permeability and leading to transudation of fluid and radiological appearance similar to left ventricular failure)
When the renal function falls below 5% of normal, the condition is termed “end stage renal failure.” The continued survival at this stage is possible only with renal transplantation. At present more than 50% of all cases of end stage renal failure are caused by diabetic nephropathy and hypertension.
 
INVESTIGATIONS 
Urine: Volume is high (2-3 liter/ 24 hr)
Mild proteinuria may present.
Most remarkable feature is the fixed specific gravity around 1010 and an osmolality of 300-m.osm/ kg water.
Presence of broad cast in urine confirms the chronic nature of illness.
Estimation of urinary loss of sodium helps to identify salt losing states. 
Blood: Blood urea, serum creatinine, serum uric acid and inorganic phosphates (Normal- 2.5 - 5 mg/dl) are elevated.
It is usual for the patient to have uraemic symptoms if the blood urea level is over 250 mg % for any length of time.
Calcium (Normal- 8.5 -10.5 mg/dl ) and bicarbonate levels (Normal- 24 -28 meq / liter) decreased.
 
X-ray: Plain x-ray of the abdomen may help if the renal size is small. 
Ultra sonogram: Help in assessing renal size.
(Normal size - 10 -12 cm length,  5 -6 cm width
3 - 4 cm thickness
Right kidney slightly smaller than the left
150 gm in adult male,  135 gin in adult female.) 
Renal—biopsy: Helps to arrive at the precise histological diagnosis.
Functions of the individual kidney can be studied in split renal function test.
The level of serum creatinine correlates with the degree of renal functional impairment as assessed by creatinine clearance. Serial estimation of serum creatinine values there for are of great help in assessing the progress of disease.
 
MANAGEMENT
Treatment of chronic renal failure is influenced by several factors and also by the stage at which the patient is first seen. The reversible complicating factors are to be identified and treated.
Water intake-- is guided by the ability of the kidney to excrete water. It is advisable to have an output of 2.5 to 3 liter/day by appropriate increase in water intake if the patient can tolerate it. The kidney can clear urea more efficiently if the urine flow rate is maintained at 2m1/ minute [around 2.5 to 3 liter/day]. Such patient can take a normal protein diet.
Sodium--Salt has to be restricted if edema, congestive cardiac failure and hypertension are present and salt should be supplemented if postural hypotension, poly urea and dehydration are present. Serum sodium should be maintained around 135 to 140 meq/liter.
Potassium—The ability of the kidney to maintain potassium balance is preserved till the patient develops advanced renal failure. At this stage potassium intake has to be restricted in order to avoid hyperkalemia. (Certain fruits, choclate, milk, vegetable and salt are rich sources of potassium)
Bicarbonate: If the serum bicarbonate level is less than 15 meq/ liters or if acidotic breathing is present bicarbonate should be supplemented.
Diet---Adequate calories have to be provided by a diet containing carbohydrate and fat. It is important to adjust the intake of protein according to the renal reserve. Since the moderate or high protein in take causes greater demand on the nephron and lead to progressive damage of partially damaged nephron. The patient approach is to restrict protein intake to 0.6 gm/kg body weight or even less. [First class protein are preferred —egg, meat, cereal etc.]
Haematological problems— Symptomatic anaemia with Haemoglobin less than 7g/dl or Packed cell volume less than 18% has to be corrected by packed cell transfusion. Factors, which aggravate the anaemia such as nutritional inadequacy and blood loss, should be corrected.
Hypertension— Fluid over load hypertension often associated with edema and sodium retension responding to salt restriction and diuretics.
In the case of hypertension in which there is no edema, the renine - angiotensin system may play the major role respond better to beeta adrenergic blocking drugs.
Hyper phosphatemia-- can be prevented by giving diet low in phosphate. Milk and dairy products, which are rich in phosphorus, are to be avoided.
Dietary supplement of calcium together with vitamin D have to be given to elevate calcium level and abolish symptoms of hypocalcaemia.
Regulated, repeated dialysis therapy or renal transplantation should be considered in end stage renal failure.
Transfusion should be avoided if at all possible. Even in the absence of renal tissue some red cell production continues and haemoglobin level can usually be kept between 6 and 8 gm % without transfusion. It is occasional essential to transfuse patient with renal anaemia, but given blood tends to depress the erythropiesis already present. Multiple transfusions carry a high risk of transfusion reaction or viral hepatitis.
 
HOMOEOPATHIC MEDICINES
Uraemia in general: Ammonium carb Apis mel
Apocynum Arsenic alb Belladonna, Cannabis indica
Cantharis Carbolic acid ,Helliborus Opium
Picric acid Terebinthinum ,Urea Vertrum vird
 
Uraemic coma:
Ammonium carb Carbolic acid
Helliborus Opium
 
Uraemic convulsion:
Belladona Carbolic acid
Cicuta virosa Opium
Plumbum met Veratrum vird
 
Uraermia with headache: 
Cannabis indica Carbolic acid
Glonoine
 
Uraernia with vomiting:
Arsenic album
Nux vomica