Thursday, November 27, 2014

Parkinson's Disease

Dictionary Meaning -
(according to Dorland's pocket medical Dictionary)

Parkinsonism - a group of neurological disorders marked by hypokinesia, tremor, and muscular rigidity, including the parkinsonian syndrome and parkinson disease.

Pathological Point Of View -
  • The motor symptoms of Parkinson's disease result from the death of dopamine-generating cells in the substantia nigra, a region of the midbrain; the cause of this cell death is unknown. 
  • Early in the course of the disease, the most obvious symptoms are movement-related; these include shaking, rigidity, slowness of movement and difficulty with walking and gait. Later, thinking and behavioral problems may arise, with dementia commonly occurring in the advanced stages of the disease, whereas depressionis the most common psychiatric symptom. Other symptoms include sensory, sleep and emotional problems. 
  • Parkinson's disease is more common in older people, with most cases occurring after the age of 50.
  • The main motor symptoms are collectively called parkinsonism, or a "parkinsonian syndrome". Parkinson's disease is often defined as a parkinsonian syndrome that is idiopathic (having no known cause), although some atypical cases have a genetic origin. 
  • Many risk and protective factors have been investigated: the clearest evidence is for an increased risk of PD in people exposed to certain pesticides and a reduced risk in tobacco smokers. 
  • Lewy bodies are the pathological hallmark of the idiopathic disorder, and the distribution of the Lewy bodies throughout the Parkinsonian brain varies from one individual to another. 
  • The anatomical distribution of the Lewy bodies is often directly related to the expression and degree of the clinical symptoms of each individual. Diagnosis of typical cases is mainly based on symptoms, with tests such as neuroimaging being used for confirmation.
  • Modern treatments are effective at managing the early motor symptoms of the disease, mainly through the use of levodopa and dopamine agonists. 
  • As the disease progresses and dopaminergic neurons continue to be lost, these drugs eventually become ineffective at treating the symptoms and at the same time produce a complication called dyskinesia, marked by involuntary writhing movements. 
  • Diet and some forms of rehabilitation have shown some effectiveness at alleviating symptoms. Surgery and deep brain stimulation have been used to reduce motor symptoms as a last resort in severe cases where drugs are ineffective. 
  • Research directions include investigations into new animal models of the disease and of the potential usefulness of gene therapy, stem cell transplants and neuroprotective agents. Medications to treat non-movement-related symptoms of PD, such as sleep disturbances and emotional problems, also exist.
  • The disease is named after the English doctor James Parkinson, who published the first detailed description in An Essay on the Shaking Palsy in 1817. Several major organizations promote research and improvement of quality of life of those with the disease and their families. Public awareness campaigns include Parkinson's disease day (on the birthday of James Parkinson, 11 April) and the use of a red tulip as the symbol of the disease. People with parkinsonism who have increased the public's awareness of the condition include actor Michael J. Fox, Olympic cyclist Davis Phinney, and professional boxerMuhammad Ali. Parkinson's not only affects humans, but other primates as well, which have often been used in researching the disease and testing approaches to its treatment.
Causes :-

Pathophysiology :-



Signs & Symptoms :-



Classification :-
Parkinsonian syndromes can be divided into four subtypes according to their origin —
  1. primary or idiopathic
  2. secondary or acquired
  3. hereditary parkinsonism, and
  4. Parkinson plus syndromes or multiple system degeneration.

I. Drug-induced Parkinsonism

  • Side effects of some drugs, especially those that affect dopaminelevels in the brain, can actually cause symptoms of Parkinsonism.
  • Although tremor and postural instability may be less severe, this condition may be difficult to distinguish from Parkinson’s disease.
  • Medications that can cause the development of Parkinsonism include:
    • Antipsychotics
    • Metaclopramide
    • Reserpine
    • Tetrabenazine
    • Some calcium channel blockers
    • Stimulants such as amphetamines and cocaine
    • Usually after stopping those medications Parkinsonism gradually disappears

II. Progressive Supranuclear Palsy (PSP)

  • PSP is one of the more common forms of atypical Parkinsonism.
  • Symptoms of PSP usually begin after age 50 and progress more rapidly than PD.
  • These symptoms include: imbalance, frequent falls, rigidity of thetrunk, voice and swallowing changes and (eventually) eye-movement problems including the ability to move eyes up and down.
  • Dementia develops later in the disease. There is no specific treatment for PSP.
  • Dopaminergic medication treatment is often tried and may provide some benefit.
  • Other therapies such as speech therapy, physical therapy, andantidepressants are important for management of patients with PSP.
  • No laboratory/brain scan testing exists for PSP. In rare cases, some patients may have shrinking of a particular part of the brain, called the “Pons”, which can be seen on an MRI of the brain.

III. Corticobasal Degeneration (CBD)

  • CBD is the least common of the atypical causes of Parkinsonism
  • CBD develops after age 60 and progresses more rapidly than PD.
  • The initial symptoms of CBD include asymmetric bradykinesia, rigidity, limb dystonia, postural instability, and disturbances of language.
  • There is often marked and disabling apraxia of the affected limb, where it becomes difficult or impossible to control the movements of the affected limb even though there is no weakness or sensory loss.
  • No laboratory/brain scan tests exist to confirm the diagnosis of CBD. CBD is a clinical diagnosis.
  • There is no specific treatment for CBD.
  • Supportive treatment such as botulinum toxin (Botox) for dystonia, antidepressants, speech and physical therapy may be helpful.
  • Levodopa and dopamine agonists (common PD medications) seldom help.

IV. Multiple System Atrophy (MSA)

  • MSA is a larger term for several disorders in which one or more system in the body deteriorates.
  • Included in the category of MSA are: Shy-Drager syndrome (DSD), Striatonigral degeneration (SND) and OlivoPontoCerebellar Atrophy (OPCA).
  • The mean age of onset is in the mid-50s.
  • Symptoms include: bradykinesia, poor balance, abnormal autonomic function, rigidity, difficulty with coordination, or a combination of these features.
  • Initially, it may be difficult to distinguish MSA from Parkinson’s disease, although more rapid progression, poor response to common PD medications, and development of other symptoms in addition to Parkinsonism, may be a clue to its diagnosis.
  • No laboratory/brain scan testing exists to confirm the diagnosis of MSA.
  • Patients respond poorly to PD medications, and may require higher doses than the typical PD patient for mild to modest benefits.

V. Vascular Parkinsonism

  • Multiple small strokes can cause Parkinsonism.
  • Patients with this disorder are more likely to present with gait difficulty than tremor, and are more likely to have symptoms that are worse in the lower part of the body.
  • Some will also report the abrupt onset of symptoms or give a history of step-wise deterioration (symptoms get worse, then plateau for a period).
  • Dopamine is tried to improve patients’ mobility although the results are often not as successful. 
  • Vascular Parkinsonism is static (or very slowly progressive) when compared to other neurodegenerative disorders.

VI. Dementia with Lewy bodies (DLB)

  • DLB is a neurodegenerative disorder that results in progressive intellectual and functional deterioration.
  • Patients with DLB usually have early dementia, prominent hallucinations, fluctuations in cognitive status over the day, and Parkinsonism.
  • Cognitive changes in patients with DLB include deficits in attention, executive function (problem solving, planning) and visuospacial function (the ability to produce and recognize figures, drawing or matching figures).
  • There are no known therapies to stop or slow the progression of DLB.
Management :-


Treatment in Homoeopathy :-
" One Single Simple Drug Substance In Its Most Suitable Potency, According To Symptom Similarity Based On Totality! "

In Case Of Parkinson's Disese, List Of Useful Remedies (According To REPERTORY
by Oscar E. BOERICKE, M.D.) Are As Below-



Agitans -- Agar., Ars., Aur. sul., Avena, Bufo, Camph. monobr., Can. ind., Cocaine, Cocc., Con., Dub., Gels., Helod., Hyos., Hyosc. hydrobr., Kali br., Lathyr., Lolium, Mag. p., Mang. ac., Merc. s., Merc., Nicotine, Phos., Physos., Plumb., Scutel., Tab., Tar. h., Zinc. cy., Zinc. picr.


 Some Examples Are :-

 Mercurius

Weakness of limbs, trembling of extremities, especially hands. Paralytic agitans. Lacerating pain in joints. Cold and clammy sweat on limbs. Oily perspiration.Tremors everywhere in body. Weakness with trembling from least exertion. All symptoms are aggravated at night, warmth of bed, Damp, cold, rainy weather and during perspiration. Complaints increase during sweating and rest. All symptoms always associated with weariness, prostration and trembling.
Slow in answering questions. Memory weakened and loss of will power. Skin alwaysmoist and freely perspiring. Itching worse warmth of bed.
Zincum-Metallicum
Violent trembling (twitching) of the whole body especially after emotions. Twitching in children. Chorea.  Paralysis of hands and feet. Trembling of hands while writing. Lameness, weakness, trembling and twitching of various muscles. Feet in continued motion, cannot keep still. Worse touch, between 5-7 pm., after dinner, better eating, discharges.
Rhus-tox
When the tremors start with pain which is relieved by motion. There is stiffness of the parts affected. Numbness and formication, after overwork and exposure. Paralysis; trembling after exertion. Limbs stiff and paralysed.All joints hot and painful. Crawling and tingling sensation in the tips of fingers. Worse during sleep, cold, wet rainy weather and after rain, night, during rest, drenching and when lying on back or right side. Better warm, dry weather, motion, walking, change of position, rubbing, stretching out limbs.
Gelsemium
Centers its action on nervous system, causing various degrees of motor paralysis…Dizziness, drowsiness, dullness and trembling are the hallmark of this remedy. Trembling ranks the highest in this remedy, weakness and paralysis, especially of the muscles of the head. Paralysis of various groups of muscles like eyes, throat, chest, sphincters and extremities. Head remedy for tremors. Mind sluggish and muscular system relaxed. Staggering gait. Loss of power of muscular control. Cramps in muscles of forearm. Excessive trembling and weakness of all limbs. Worse by dampness, excitement, bad news. Better by bending forwards, profuse urination, continued motion and open air.
Argentum Nitricum
It is complimentary to Gelsemium. Memory impaired; easily excited and angered; flatulence and greenish diarrhea.Inco-ordination, loss of control and imbalance with trembling and general debility. Paralysis with mental and abdominal symptoms. Rigidity of calves. Walks and stands unsteadily. Numbness of body. Specially arms.
Agaricus Muscarius
Trembling, itching and jerking, stiffness of muscles; itching of skin over the affected parts and extreme sensitiveness of the spine. Cannot bear touch. Jerking and trembling are strong indications. Chorea and twitching ceases during sleep. Paralysis of lower limbs with spasmodic conditions of arms. Numbness of legs on crossing them. Paralytic pain in left arm followed by palpitation. Stiffness all over with pain over hips.
Cocculus
Head trembles while eating and when it is raised higher. Knees sink down from weakness. Totters while walking with tendency to fall on one side. Cracking of the knee when moving. Lameness worse by bending. Trembling and pain in limbs. One-sided paralysis worse after sleep. Intensely painful, paralytic drawing. Limbs straightened out and painful when flexed.
It shows special affinity for light haired females especially during pregnancy.
Lathyrus
Tremors of the upper extremities with paralytic weakness of the lower limbs. Feels as if limbs are hard and contracted; limbs feel heavy. Feels as if floor is irregular and is obliged to keep his eyes on the ground to guide his feet. Affects the lateral and anterior columns of cord. Does not produce pain. Reflexes always increased. Lateral sclerosis and Infantile paralysis. Finger tips numb. Tremulous, tottering gait. Excessive rigidity of legs with spastic gait. Knees knock against each other while walking. Cannot extend or cross legs when siting.Stiff and lame ankles.
Physostigma
Marked fibrillary tremors and spasms of the muscles, worse from motion or application of cold water. Palpitation and fluttering of the heart felt throughout the body. Depresses the motor and reflex activity of the cord and causes the loss of sensibility to pain, muscle weakness and paralysis.  Paralysis and tremors, chorea. Meningeal irritation with rigidity of muscles. Pain in right popliteal space. Burning and tingling in spine. Hands and feet numb with sudden jerking of limbs on going to sleep. Crampy pain in limbs.
Ambra Grisea
Tremors with numbness, limbs go to sleep on the slightest movement, coldness and stiffness of limbs. The finger nails become brittle and are shriveled. Cramps in hands and fingers. Worse grasping anything. Cramps in legs. Extreme nervous hypersensitiveness. Dread of people and desire to be alone. Music causes weeping. One sided complains call for it.
Heloderma
Trembling along nerves in limbs. Tired feeling, very weak and nervous, fainting, numb sensation. It causes locomotor ataxia. The eyes become more prominent and corneal opacities visible. Very depressed and sensation as if would fall on right side. Sensationas if walking on sponge. As if the feet were swollen. When walking, lifts feet higher than usual and puts down heel hard. Stretching relieves pains in muscles and limbs.
Mag-phos
Trembling; shaking of hands, involuntary. Paralysis agitans. Cramps in calves, feet very tender. Twitching, Chorea, cramps. Numbness of finger tips. Worse right side, cold, touch, night. Better warmth, bending double, pressure and friction.
Bufo Rana
Special action on nervous system. Painful paralysis. Pain in loins, numbness and cramps. Staggering gait. Feels as if a peg is driven into joints. Worse—Warm room. Better bathing or cold air. Putting feet in cold water.
Tarentula
Remarkable nervous phenomena. Chorea, extreme restlessness and Paralysis agitans.Must keep in constant motion even though walking aggravates. Numbness of legs with twitching and jerkings.Extraordinary contractions and movements.
Plumbum Metalicum
Paralytic agitans. Paralysis of single muscles. Cannot raise or lift anything. Extension is difficult. Paralysis from over-exertion of extensor muscles in piano players. Wrist drop. Loss of patellar reflex. Pain in right big toe at night. Hands and feet cold. Infantile paralysis and neuritis.
Conium
Heavy, weary and paralyzed limbs. Trembling and unsteady hands. Muscular weakness especially of lower extremities. Perspiration of hands. Putting feet on chair relieves.Ascending paralysis ending in death by failure of respiration. Worse by lying down, turning or rising in bed, cold, exertion. Better by darkness, limbs hanging down, motion, pressure.
For More Details :-
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Thursday, November 20, 2014

Renal Failure

Introduction :-
  • Renal failure (also kidney failure or renal insufficiency) is a medical condition in which the kidneys fail to adequately filter waste products from the blood. 

 Classification :-

Acute kidney injury






Pathologic kidney specimen showing marked pallor of the cortex, contrasting to the darker areas of surviving medullary tissue. The patient died with acute kidney injury.






  • Acute kidney injury (AKI), previously called acute renal failure (ARF), is an abrupt loss of kidney function that develops within 7 days.

Chronic kidney disease





Uremic frost on the forehead and scalp of a young man who presented with complaints of chronic anorexia and fatigue with blood urea nitrogen and serum creatinine levels of approximately 100 and 50 mg/dL respectively.




  • Chronic kidney disease (CKD), also known as chronic renal disease (CRD), is a progressive loss in renal function over a period of months or years. 
  • Often, chronic kidney disease is diagnosed as a result of screening of people known to be at risk of kidney problems, such as those with high blood pressure or diabetes and those with a blood relative with chronic kidney disease. 
  • It is differentiated from acute kidney disease in that the reduction in kidney function must be present for over 3 months.
  • Chronic kidney disease is identified by a blood test for creatinine. Higher levels of creatinine indicate a lower glomerular filtration rate and as a result a decreased capability of the kidneys to excrete waste products. Creatinine levels may be normal in the early stages of CKD, and the condition is discovered ifurinalysis (testing of a urine sample) shows that the kidney is allowing the loss ofprotein or red blood cells into the urine. To fully investigate the underlying cause of kidney damage, various forms of medical imaging, blood tests and often renalbiopsy (removing a small sample of kidney tissue) are employed to find out if there is a reversible cause for the kidney malfunction. Recent professional guidelines classify the severity of chronic kidney disease in five stages, with stage 1 being the mildest and usually causing few symptoms and stage 5 being a severe illness with poor life expectancy if untreated. Stage 5 CKD is often called end stage renal disease (ESRD), end stage renal failure (ESRF), or end-stage kidney disease (ESKD) and is synonymous with the now outdated terms chronic kidney failure (CKF) or chronic renal failure (CRF).
  • There is no specific treatment unequivocally shown to slow the worsening of chronic kidney disease. If there is an underlying cause to CKD, such as vasculitis, this may be treated directly to slow the damage. In more advanced stages, treatments may be required for anemia and bone disease. Severe CKD requires renal replacement therapy, which may involve a form of dialysis, but ideally constitutes a kidney transplant.

Acute-on-chronic renal failure

  • Acute kidney injuries can be present on top of chronic kidney disease, a condition called acute-on-chronic renal failure (AoCRF). The acute part of AoCRF may be reversible, and the goal of treatment, as with AKI, is to return the patient to baseline renal function, typically measured by serum creatinine. Like AKI, AoCRF can be difficult to distinguish from chronic kidney disease if the patient has not been monitored by a physician and no baseline (i.e., past) blood work is available for comparison.
Signs & Symptoms :-

Symptoms can vary from person to person. Someone in early stage kidney disease may not feel sick or notice symptoms as they occur. When kidneys fail to filter properly, waste accumulates in the blood and the body, a condition called azotemia. Very low levels of azotaemia may produce few, if any, symptoms. If the disease progresses, symptoms become noticeable (if the failure is of sufficient degree to cause symptoms). Renal failure accompanied by noticeable symptoms is termed uraemia.
Symptoms of kidney failure include the following :-
  • High levels of urea in the blood, which can result in:
    • Vomiting and/or diarrhea, which may lead to dehydration
    • Nausea
    • Weight loss
    • Nocturnal urination
    • More frequent urination, or in greater amounts than usual, with pale urine
    • Less frequent urination, or in smaller amounts than usual, with dark coloured urine
    • Blood in the urine
    • Pressure, or difficulty urinating
    • Unusual amounts of urination, usually in large quantities
  • A buildup of phosphates in the blood that diseased kidneys cannot filter out may cause:
  • A buildup of potassium in the blood that diseased kidneys cannot filter out (called hyperkalemia) may cause:
    • Abnormal heart rhythms
    • Muscle paralysis
  • Failure of kidneys to remove excess fluid may cause:
    • Swelling of the legs, ankles, feet, face and/or hands
    • Shortness of breath due to extra fluid on the lungs (may also be caused by anemia)
  • Polycystic kidney disease, which causes large, fluid-filled cysts on the kidneys and sometimes the liver, can cause:
    • Pain in the back or side
  • Healthy kidneys produce the hormone erythropoietin that stimulates the bone marrow to make oxygen-carrying red blood cells. As the kidneys fail, they produce less erythropoietin, resulting in decreased production of red blood cells to replace the natural breakdown of old red blood cells. As a result, the blood carries less hemoglobin, a condition known as anemia. This can result in:
    • Feeling tired and/or weak
    • Memory problems
    • Difficulty concentrating
    • Dizziness
    • Low blood pressure
  • Normally, proteins are too large to pass through the kidneys, however, they are able to pass through when the glomeruli are damaged. This does not cause symptoms until extensive kidney damage has occurred, after which symptoms include:
    • Foamy or bubbly urine
    • Swelling in the hands, feet, abdomen, or face
  • Other symptoms include:
    • Appetite loss, a bad taste in the mouth
    • Difficulty sleeping
    • Darkening of the skin
    • Excess protein in the blood
    • With high dose penicillin, renal failure patients may experience seizures

Causes :-

Acute kidney injury


  • Acute kidney injury (previously known as acute renal failure) - or AKI - usually occurs when the blood supply to the kidneys is suddenly interrupted or when the kidneys become overloaded with toxins. Causes of acute kidney injury include accidents, injuries, or complications from surgeries in which the kidneys are deprived of normal blood flow for extended periods of time. Heart-bypass surgery is an example of one such procedure.
  • Drug overdoses, accidental or from chemical overloads of drugs such as antibiotics or chemotherapy, may also cause the onset of acute kidney injury. Unlike chronic kidney disease, however, the kidneys can often recover from acute kidney injury, allowing the patient to resume a normal life. People suffering from acute kidney injury require supportive treatment until their kidneys recover function, and they often remain at increased risk of developing future kidney failure.
  • Among the accidental causes of renal failure is the crush syndrome, when large amounts of toxins are suddenly released in the blood circulation after a long compressed limb is suddenly relieved from the pressure obstructing the blood flow through its tissues, causing ischemia. The resulting overload can lead to the clogging and the destruction of the kidneys. It is areperfusion injury that appears after the release of the crushing pressure. The mechanism is believed to be the release into the bloodstream of muscle breakdown products – notably myoglobin, potassium, and phosphorus – that are the products of rhabdomyolysis (the breakdown of skeletal muscle damaged by ischemic conditions). The specific action on the kidneys is not fully understood, but may be due in part to nephrotoxic metabolites of myoglobin.

Chronic kidney disease

  • Chronic Kidney Disease (CKD) has numerous causes. The most common causes of CKD are diabetes mellitus and long-term, uncontrolled hypertension. Polycystic kidney disease is another well-known cause of CKD. The majority of people afflicted with polycystic kidney disease have a family history of the disease. Other genetic illnesses affect kidney function, as well.
  • Some infectious diseases, such as hantavirus, can attack the kidneys, causing kidney failure.

Genetic predisposition

  • The APOL1 gene has been proposed as a major genetic risk locus for a spectrum of nondiabetic renal failure in individuals of African origin, these include HIV-associated nephropathy (HIVAN), primary nonmonogenic forms of focal segmental glomerulosclerosis, and hypertension affiliated chronic kidney disease not attributed to other etiologies. Two western African variants in APOL1 have been shown to be associated with end stage kidney disease in African Americans and Hispanic Americans.

Diagnostic Approach :-

Measurement for AKI

Acute kidney injury is diagnosed on the basis of clinical history and laboratory data. A diagnosis is made when there is rapid reduction in kidney function, as measured by serum creatinine, or based on a rapid reduction in urine output, termed oliguria.

Classic laboratory findings in AKI
TypeUOsmUNaFeNaBUN/Cr
Prerenal>500<10<1%>20
Intrinsic<350>20>2%<15
Postrenal<350>40>4%>15

Definition

Introduced by the KDIGO in 2012, specific criteria exist for the diagnosis of AKI.
AKI can be diagnosed if any one of the following is present:
  • Increase in SCr by ≥0.3 mg/dl (≥26.5 μmol/l) within 48 hours; or
  • Increase in SCr to ≥1.5 times baseline, which have occurred within the prior 7 days; or
  • Urine volume < 0.5 ml/kg/h for 6 hours.

Staging

The RIFLE criteria, proposed by the Acute Dialysis Quality Initiative (ADQI) group, aid in the staging of patients with AKI:
  • Risk: 1.5-fold increase in the serum creatinine, or glomerular filtration rate (GFR) decrease by 25 percent, or urine output <0.5 mL/kg per hour for six hours.
  • Injury: Twofold increase in the serum creatinine, or GFR decrease by 50 percent, or urine output <0.5 mL/kg per hour for 12 hours
  • Failure: Threefold increase in the serum creatinine, or GFR decrease by 75 percent, or urine output of <0.3 mL/kg per hour for 24 hours, or anuria for 12 hours
  • Loss: Complete loss of kidney function (e.g., need for renal replacement therapy) for more than four weeks
  • End-stage renal disease: Complete loss of kidney function (e.g., need for renal replacement therapy) for more than three months

Measurement for CKD


Stages of kidney failure
  • Chronic kidney failure is measured in five stages, which are calculated using a patient’s GFR, or glomerular filtration rate. 
  • Stage 1 CKD is mildly diminished renal function, with few overt symptoms. 
  • Stages 2 and 3 need increasing levels of supportive care from their medical providers to slow and treat their renal dysfunction. 
  • Patients in stages 4 and 5 usually require preparation of the patient towards active treatment in order to survive. Stage 5 CKD is considered a severe illness and requires some form of renal replacement therapy (dialysis) or kidney transplant whenever feasible.

Glomerular filtration rate
CKD StageGFR level (mL/min/1.73 m2)
Stage 1≥ 90
Stage 260 – 89
Stage 330 – 59
Stage 415 – 29
Stage 5< 15
  • A normal GFR varies according to many factors, including sex, age, body size and ethnic background. Renal professionals consider the glomerular filtration rate (GFR) to be the best overall index of kidney function. The National Kidney Foundation offers an easy to use on-line GFR calculator for anyone who is interested in knowing their glomerular filtration rate. (A serum creatinine level, a simple blood test, is needed to use the calculator).

Use of the term uremia

  • Before the advancement of modern medicine, renal failure was often referred to as uremic poisoning. Uremia was the term for the contamination of the blood with urine. It is the presence of an excessive amount of urea in blood. Starting around 1847, this included reduced urine output, which was thought to be caused by the urine mixing with the blood instead of being voided through the urethra. The term uremia is now used for the illness accompanying kidney failure.
Management :-

In Morden Medicine
  • The management of AKI hinges on identification and treatment of the underlying cause. In addition to treatment of the underlying disorder, management of AKI routinely includes the avoidance of substances that are toxic to the kidneys, called nephrotoxins. These include NSAIDs such as ibuprofen, iodinated contrasts such as those used for CT scans, many antibiotics such as gentamicin, and a range of other substances.
  • Monitoring of renal function, by serial serum creatinine measurements and monitoring of urine output, is routinely performed. In the hospital, insertion of a urinary catheter helps monitor urine output and relieves possible bladder outlet obstruction, such as with an enlarged prostate.

Specific therapies

  • If the cause is obstruction of the urinary tract, relief of the obstruction (with a nephrostomy or urinary catheter) may be necessary.

Diuretic agents

  • The use of diuretics such as furosemide, is widespread and sometimes convenient in ameliorating fluid overload. It is not associated with higher mortality (risk of death), nor with any reduced mortality or length of intensive care unit or hospital stay.

Renal replacement therapy








A hemodialysis machine, used to physiologically aid or replace the kidneys in renal failure



Treatment in Homoeopathy :-

" One Single Simple Drug Substance In Its Most Suitable Potency, According To Symptom Similarity Based On Totality! "
Aconite
Incipient stage of post scarlatinal nephritis, pain in loins, scanty urine without blood.

 Apis mellifica
Apis is not so much a remedy for chronic Bright’s disease as for the acuter forms. There are oedematous swellings of the face and extremities, paleness, ascites, oedema pulmonum, pains in the head, back and limbs. Albuminuria following scarlatina. It may be of use in any form of Bright’s disease when there are dull pains in the kidneys, scanty urine and frequent Micturition. The urine is heavily charged with albumen and contains blood corpuscles. The oedema appears quickly, there is general dropsy and suppression of urine and perhaps an eruption of the skin like a nettle rash. The patient  is drowsy, apathetic and has a bruised feeling all over. Apis in such cases acts best in trituration; do not depend on the tincture or dilutions. Hepar is recommended by Kafka in Bright’s disease following scarlatina. A valuable symptom for Apis is the feeling of suffocation. He does not see how he is get another breath.

 Apocynum
Palliative in dropsical conditions where the urine is scanty. Also useful for coma & convulsions in the nephritis of pregnency.

 Arsenicum
This remedy corresponds to all stages of Bright’s disease, bearing a closer resemblance than any other remedy. It comes in later in the disease where there is dropsy, pale skin, waxen appearance, watery diarrhea and great thirst. The urine is dark, casts are abundant, and it contains much albumen. There are attacks of dyspnoea when lying down in the evening and after midnight, relieved by an expectoration of mucus. It may come in immediately after Aconite in many cases. “Blood boils” make a special indication for this remedy. Baehr, Millard and Hale question the usefulness of Arsenicum in kidney affections. However, it seems a simile to the large white kidney; in fact, one could hardly wish for a closer correspondence. Hughes considers it a favorite with anxiety and sinking of vital forces will call for Arsenicum. Calcarea arsenica has been used in the anaemia, progressive emaciation and debility of this disease with success.

 Aurum muriaticum
Morbus Brightii from gout, suppurations or syphilis. Interstitial nephritis in its incipiency with digestive and nervous phenomena, hypochondriasis, irritability and vertigo.

 Belladonna
Simple albuminuria, here it seems to occupy a place midway between Aconite and Arsenicum. Belladonna is of the greatest service in inflammation of the kidneys with piercing  burning pains in the lumbar region, returning periodically with increased severity.

 Cantharis
This remedy pictures nephritis with cutting pains in the lumbar region; the urine is passed in drops and is mixed with blood, with much urging. Post scarlatinal and post diphtheric kidney diseases with dropsy may indicate Cantharis.

 Convallaria
Nephritis from heart disorders. It affords relief when there is extreme rapid & irregular action of the heart, and in general anasarca & ascites from mitral insufficiency.

 Cuprum arsenicum
Cuprum arsenicum is also useful in uraemic conditions and is praised highly by Goodno. Cuprum is a valuable remedy for uraemic eclampsia.

 Digitalis
This remedy has an irritant action on the kidneys. It is homoeopathic to granular degeneration. Heart symptoms, feeble pulse, scanty, dark, turbid urine, faintness at the stomach, rheumatic pains will indicate it. It is especially useful when the circulation is weak. Rheumatic pains, pulmonary catarrh with profuse expectoration are marked symptoms.

 Glonoine
Glonoine has albuminous urine and will sometimes be found useful in acute and haemorrhagic nephritis.

 Kali chloricum
This remedy is said to be the most homoeopathic of all remedies in Bright’s disease. It has scanty, dark, albuminous urine containing casts. It excites a violent nephritis.

 Mercurius corrosivus
This remedy corresponds to the large white kidney. There is an albuminous, scanty and red urine; pale waxen color of the body; there are lumbar pains, great dyspnoea and excessive strangury. It takes the first rank among all the mercurials for nephritis, and it comes in the later stages. Syphilitic complication further indicate it. There is an expression of uneasiness on the face. Dr. Ludlam considers it our best remedy for the albuminous nephritis of pregnancy and Baehr lauds it in suppurative nephritis.

 Plumbum
Granular degenerations of the kidneys, with tendency to uraemic convulsion. Dropsy, sallow face, emaciation, oedema about the ankles. It seems to corresponds to the contracted or cirrhotic form of nephritis, holding the same relation here that Arsenic and Mercury do in chronic nephritis. Royal emphasizes this remedy saying that it arrested the progress in many cases and permanently cured not few for him.

 Phosphorus
Phosphorus produces as marked a nephritis as any drug. It is one of the most important remedies in Bright’s disease; the characteristic symptoms are: lassitude of  the whole body, hands and feet icy cold, sleepiness. The fatigue is greatest in the morning, and there is heat in the body without thirst, especially in the evening. The patient is indisposed to work, is giddy, forgetful and has a heavy headache, particularly in the forehead; there is oedema of the upper eyelids, a mist before the eye, a yellowish fray complexion, a sickly oedema of the face, want of appetite, pressure and burning in the stomach, and a light colored painless diarrhea which is very weakening. It suits well fatty or waxy casts, is dark brown, scanty and albuminous, or covered with an iridescent film. Pulmonary complications will call for Phosphorus; and inability to lie on the left side is a prominent symptom in these cases. Vomiting and gastric symptoms are usually present. A small dose of Phosphorus will act much safer and better in eclampsia than a large dose of Morphine.

 Terebinth

One of our reliable and most frequently indicated remedies in the early stages of renal diseases when congestion is prominent, when there is much pain in the back of a  dull character extending along the ureters. The great characteristic of dark smoky urine will be present. There is anasarca, and of course, the urine is bloody and albuminous. It is recommended in post scarlatinal renal affections. The prostration is  not accompanied by the restlessness of Arsenicum.

& The List Goes On.....


Ultimately similimum can only be found by taking totality of the symptoms as per the individual case.
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With Best Regards, Karnav Thakkar :) :)

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