Role Of Homoeopathic Medicines In Acute Kidney Injuries - homeopathy360

Role Of Homoeopathic Medicines In Acute Kidney Injuries

Acute kidney injury (AKI) (formerly acute renal failure) is the syndrome arising from a rapid fall in GFR (over hours to days). Acute kidney injury (AKI) is defined by the impairment of kidney filtration and excretory function over days to weeks, resulting in the retention of nitrogenous and other waste products normally cleared by the kidneys. AKI is not a single disease but, rather, a designation for a heterogeneous group of conditions that share common diagnostic features. It is important to recognize that AKI is a clinical diagnosis and not a structural one. A patient may have AKI with or without injury to the kidney parenchyma. AKI can range in severity from asymptomatic and transient changes in laboratory parameters of glomerular filtration rate (GFR), to overwhelming and rapidly fatal derangements in effective circulating volume regulation and electrolyte and acid-base composition of the plasma.
It is characterized by retention of both nitrogenous (including Ur and Cr) and non-nitrogenous waste products of metabolism, as well as disordered electrolyte, acid – base, and fluid homeostasis.
There is evidence that even relatively small acute reductions in kidney function are associated with poorer outcomes, including increased mortality, higher risk of long-term dialysis, and longer hospital stay.
Historical limitations: –
• Despite a relative insensitivity to acute changes in GFR, most definitions of acute renal dysfunction have been based on serum Cr, either as an absolute value or as a change from baseline. Other definitions have incorporated urine output (UO) or the need for dialysis support.
• A 2004 survey of 598 participants at a critical care nephrology conference revealed 199 different criteria to define AKI and 90 for the initiation of renal replacement therapy.
The RIFLE criteria for AKI: –
• In response, the Acute Dialysis Quality Initiative established a multi-layered definition of AKI called the RIFLE criteria.
• AKI is stratified into five stages, based on severity and duration of renal injury: Risk, Injury, Failure, Loss, and End-stage disease (see Table 1).
• Many studies (>0.5 million patients) have validated these criteria.
• RIFLE-defined AKI is associated with significantly reduced survival (with increasing RIFLE stage leading to greater risk of death).
RIFLE category SCr/GFR criteria Urine output criteria
Risk increase S. Cr ≥ 150 – 200% (1.5 – 2-fold) OR decrease of GFR >25% 200 – 300% (>2 – 3-fold) OR decrease of GFR >50% 300% (>3-fold) from baseline OR decrease of GFR >75% OR SCr≥350μmol/L (≥4.0mg/dL) with an acute rise of at least 45μmol/L (0.5mg/dL). Or on RRT. 4 weeks
End stage disease Need for RRT for >3 months

Acute Kidney Injury Network (AKIN) classification: –
• More recently, AKIN (an international network of AKI experts) modified RIFLE to incorporate small changes in S.Cr occurring within a 48h period and to remove changes in GFR as diagnostic criteria (see Table 2)
AKIN stage Serum creatinine criteria Urine output criteria
1 SCr ≥26.4μmol/L (0.3mg/dL) in ≤48h OR i SCr ≥150 – 200% (1.5 – 2-fold) from baseline 6 hours
2 SCr >200 – 300% (2 – 3-fold) from baseline 12 hours
3 SCr ≥300% (3-fold) from baseline OR SCr ≥354μmol/L (>4mg/dL) with an acute rise of ≥44μmol/L (0.5mg/dL) OR treatment with RRT < 0.3 mL/kg/hr for 24 hours OR
Anuria for 12 hours

KDIGO AKI definition (2012): –
• AKI, classified by either of the earlier listed criteria, may identify slightly different patients:
RIFLE may not detect 7-10% of AKIN-identified cases,
and AKIN may miss 7.25% RIFLE cases.
• KDIGO have recently produced a definition that incorporates the key elements of both, and it is likely that this definition will become the accepted standard.
Key elements of KDIGO AKI definition
• Increase in SCr by ≥ 26.5μmol/L (≥ 0.3mg/dL) within 48h.
• Increase in SCr by ≥ 1.5 x baseline (known or presumed to have occurred within prior 7d).
• Urine volume elective (25% vs < 5% AKI).
Hepatic and biliary surgery (over 70% of hepatic transplants complicated by AKI); biliary surgery also high risk.
• Diabetes mellitus (esp. if established diabetic nephropathy with d eGFR).
• Volume depletion (NBM, bowel obstruction, vomiting, burns).
• LV dysfunction and other cardiac disease.
• Other causes of decreased effective arterial volume (cirrhosis).
Drugs that cause renal vasomotor changes (NSAIDs, ACE-I, ARB).
Hyperbilirubinemia and frank jaundice.
Multiple myeloma (may just be that these patients are often dehydrated, with a degree of renal insufficiency to start with). Precipitation of casts with tubular injury is the concern.

Clinical Features: –
Patients may be asymptomatic during the early stages of AKI, despite nearly non-functioning kidneys, and may be very unwell by the time the diagnosis is apparent (emphasizing why it is so important to be familiar with high-risk patients and high-risk situations)
Presenting features of AKI
• High Urea and high S. Creatinine.
• decreased Urine Output (UO <400mL/d is frequent ~50%, but not invariable)
• Volume depletion OR
• Volume overload leading to pulmonary oedema.
• Hyperkalaemia (leading to arrhythmias or cardiac arrest).
• Non-specifically sick, often deteriorating, patient.
Rarely, • Uremic symptoms
Check renal function and K + in all acutely unwell patients, esp. if:
• Falling or low UO, or anuria.
• Persistent nausea and vomiting, or prolonged NBM.
• Drowsiness or impaired conscious level.
• Signs of systemic sepsis.
• Hypertension or hypotension, particularly if severe.
• Pulmonary +- peripheral oedema.
• Puzzling ECG abnormalities (T wave changes and conduction delays).
• Metabolic acidosis.
Lab findings: –
Err on the side of caution (i.e. assume AKI until proven otherwise).
• In many situations, particularly when renal size is normal, a kidney biopsy may be necessary to determine the nature of the renal lesion and the extent of reversibility.
• CBC:
• decreased Hb develops early, typically 80–100g/L.; Haemolysis, GI bleeding.
• increased WBC: infection (rarely tissue infarction or vasculitis).
Eosinophilia is a rare feature of TIN and cholesterol emboli.
decreased WBC: severe sepsis (rarely SLE).
• decreased platlates: DIC or thrombotic microangiopathy
increased platlates: inflammatory disorder, e.g. vasculitis.
• Pancytopenia: marrow infiltration (? myeloma or other malignancy).
• Clotting:
• ? Liver disease (increased INR) or DIC (increased PT, increased APTT, increased D-dimers). • Group and save if anaemic.
• increased ESR with any inflammatory condition but esp. myeloma and SLE.
• Blood film if decreased platlates or? microangiopathy:
• Fragmented red cells. If found, send LDH, haptoglobins, reticulocyte count.
• Urine & Electrolytes:
• increased plasma Urea: Creatinine ratio may indicate pre-renal AKI
• increased K +. Needed urgently.
• Na + usually normal; decreased Na + occurs if volume overload or diuretics.
• decreased venous HCO 3 – leads to metabolic acidosis (if normal with normal O 2 saturation, then ABG may not be necessary).
• LFTs:
• decreased albumin may imply proteinuria and GN.
•? increased bilirubin, ? hepatorenal syndrome ,? paracetamol overdose.
• increased transaminases may be of muscle origin leads to check the CK.
• Ca 2+ and PO 4:
• increased Ca 2+ is a cause of AKI (? myeloma, sarcoidosis, malignancy).
•decreased Ca 2+ and increased PO4 are present in most cases.
• CRP for infection or inflammation. Procalcitonin if available.
• Creatine kinase (CK) if rhabdomyolysis likely.
• Urate if tumour lysis or pre-eclampsia possible.
• Lactate to assess tissue ischaemia or under perfusion.
Microbiology Culture urine and blood if any clinical suspicion of sepsis.
Arterial blood gas ABG and lactate are necessary if venous HCO 3 – is low (or unavailable) or there is evidence of sepsis, hypotension, or clinical deterioration.
Radiological investigations include-
1 Chest X ray PA view
2 Ultrasound:
• Long-standing renal disease leads to loss of renal parenchyma and decreased renal size.
• Small (< 9 – 10cm length), echo bright, often cystic kidneys are characteristic of CKD.
2 Normal-sized kidneys should arouse suspicion of AKI.
A common exception is diabetic nephropathy.
Renal biopsy is also done in some cases.
Management: –
Many cases of AKI can be prevented or reversed at an early stage.
Three principles
1. Avoid dehydration.
2. Avoid nephrotoxins (IV contrast, NSAIDs, aminoglycosides).
3. Review clinical (esp. volume) status and renal function if at risk.
AKI is a type of chronic miasmatic disease, especially of intrinsic type of AKI.
Some symptoms may also be caused due to some exciting cause like hypovolaemia due to haemorrhage, trauma, post op, excessive diarrhoea- vomiting; Here, Fluid replacement has to be done in severe cases.
In cases of Acute renal failure, one should assess the general condition of the patient & rule out the cause as it is an emergency condition & treat as per presenting symptoms till the patient settles.
In cases where it is due to some nephrotoxic drugs like overuse of NSAIDs, ACE-I, ARB etc, are to be withdraw as soon as possible.
§ 78 Fifth Edition
The true natural chronic diseases are those that arise from a chronic miasm, which when left to themselves, and unchecked by the employment of those remedies that are specific for them, always go on increasing and growing worse, notwithstanding the best mental and corporeal regimen, and torment the patient to the end of his life with ever aggravated sufferings.
These are the most numerous and greatest scourges of the human race; for the most robust constitution, the best regulated mode of living and the most vigorous energy of the vital force are insufficient for their eradication.
These mostly covers Sycotic & sometimes Syphilitic miasm in background.
§ 79
Hitherto syphilis alone has been to some extent known as such a chronic miasmatic disease, which when uncured ceases only with the termination of life. Sycosis (the condylomas disease), equally ineradicable by the vital force without proper medicinal treatment, was not recognized as a chronic miasmatic disease of a peculiar character, which it nevertheless undoubtedly is, and physicians imagined they had cured it when they had destroyed the growths upon the skin, but the persisting dyscrasia occasioned by it escaped their observation.
Sometimes they may be acute exacerbation of chronic disease. In such conditions as per § 92
But if it be a disease of a rapid course, and if its serious character admit of no delay, the physician must content himself with observing the morbid condition, altered though it may be by medicines, if he cannot ascertain what symptoms were present before the employment of the medicines, – in order that he may at least form a just apprehension of the complete picture of the disease in its actual condition, that is to say, of the conjoint malady formed by the medicinal and original diseases, which from the use of inappropriate drugs is generally more serious and dangerous than was the original disease, and hence demands prompt and efficient aid; and by thus tracing out the complete picture of the disease he will be enabled to combat it with a suitable homoeopathic remedy, so that the patient shall not fall a sacrifice to the injurious drugs he was swallowed.

Apis Melifica: – Acts on cellular tissues causing oedema of skin and mucous membranes. Swelling or puffing up of various parts, oedema, red rosy hue, stinging pains, soreness, intolerance of heat, and slightest touch, and afternoon aggravation are some of the general guiding symptoms. Thirst less; Burning and soreness when urinating. Suppressed, loaded with casts; frequent and involuntary; stinging pain and strangury; scanty, high coloured. Incontinence. Last drops burn and smart. Worse, heat in any form; touch; pressure; late in afternoon; after sleeping; in closed and heated rooms. Right side. Better, in open air, uncovering, and cold bathing.
Apocynum: – Increases secretions of mucous and serous membranes and acts on cellular tissue, producing oedema and dropsy and on skin causing diaphoresis.; diminished frequency of pulse; Bladder much distended. Turbid, hot urine, with thick mucus and burning in urethra, after urinating. Little expulsive power. Dribbling. Strangury. Renal Dropsy.
Acid Benz: – uric acid diathesis, with urine highly coloured and very offensive, and gouty symptoms. Renal insufficiency. Pains suddenly change their locality. Repulsive odour; changeable colour; brown, acid. Enuresis; dribbling, offensive urine of old men. Excess of uric acid. Cystitis. Worse, motion, standing
Acid Nitric: – Scanty, dark, offensive. Smells like horse’s urine. Cold on passing. Burning and stinging. Urine bloody and albuminous. Alternation of cloudy, phosphatic urine with profuse urinary secretion in old prostatic cases. Worse, evening and night, cold climate, and also hot weather. Better, while riding in carriage
Berberis vulgaris: – Rapid change of symptoms-pains change in regard to place and character-thirst alternates with thirst lessness, hunger, and loss of appetite; arthritic affections with urinary disturbances. Wandering, radiating pains. Burning pains. Sensation as if some urine remained after urinating. Urine with thick mucus and bright-red, mealy sediment. Bubbling, sore sensation in kidneys. Pain in bladder region. Pain in the thighs and loins on urinating. Frequent urination; urethra burns when not urinating. Worse, motion, standing. It brings on, or increases, urinary complaints.
Belladonna: – Belladonna stands for violence of attack and suddenness of onset. Useful in hypertensive emergencies. Vertigo, with falling to left side or backwards. Sensitive to least contact. Much throbbing and heat. fullness, especially in forehead, also occiput, and temples. Retention of urine. Acute urinary infections. Sensation of motion in bladder as of a worm. Urine scanty, with tenesmus; dark and turbid, loaded with phosphates. Worse, touch, jar, noise, draught, after noon, lying down. Better, semi-erect.
Cantharis: – Over sensitiveness of all parts. Irritation. Raw, burning pains. Haemorrhages. Intolerable, constant urging to urinate; Intolerable urging and tenesmus. Nephritis with bloody urine. Violent paroxysms of cutting and burning in whole renal region, with painful urging to urinate; bloody urine, by drops. Intolerable tenesmus; cutting before, during, and after urine. Urine scalds him, and is passed drop by drop. Constant desire to urinate. Membranous scales looking like bran in water. Urine jelly-like, shreddy. Worse, from touch, or approach, urinating, drinking cold water or coffee. Better, rubbing.
HELLEBORUS NIGER: – general muscular weakness; useful in low states of vitality and serious disease. Suppressed; scanty, dark; coffee-grounds sediment. Frequent urging. Bladder overdistended. Worse, from evening until morning, from uncovering.
Ipecac: – persistent nausea and vomiting, Moorages bright-red and profuse. Worse, periodically; from veal, moist warm wind, lying down.; Pre renal AKI
Litres S: – Renal dropsy. Here the suppressed urination is most favourably influenced. General anasarca due to heart and kidney disease. Diarrhoea with violent urging and pain in lower part of back. Colic. Locally, applied to ulcers and unhealthy wounds. A prompt diuretic.
Medorrhinum: – A powerful and deep-acting medicine, often indicated for chronic ailments due to suppressed gonorrhoea. Oedema of limbs; dropsy of serous sacs. Painful tenesmus when urinating. Renal colic; Urine flows very slowly. Worse, when thinking of ailment, from daylight to sunset, heat, inland. Better, at the seashore, lying on stomach, damp weather.
Nat Mur: – symptoms of salt retention as evidenced by dropsies and oedemas; an alteration in the blood causing a condition of anćmia and leucocytosis. There seems also to be a retention in the tissues of effected materials giving rise to symptoms loosely; Dry mucous membranes; Great weakness and weariness. Pain just after urinating. Increased, involuntary when walking, coughing, etc. Has to wait a long time for it to pass if others are present.; Worse, noise, music, warm room, lying down about 10 am; at seashore, mental exertion, consolation, heat, talking. Better, open air, cold bathing, going without regular meals, lying on right side; pressure against back, tight clothing.
Nux Vomica: – Irritable bladder; from spasmodic sphincter. Frequent calls; little and often. Haematuria. Ineffectual urging, spasmodic and strangury. Renal colic extending to genitals, with dribbling urine. While urinating, itching in urethra and pain in neck of bladder. Post renal AKI; Worse, morning, mental exertion, after eating, touch, spices, stimulants, narcotics, dry weather, cold. Better, from a nap, if allowed to finish it; in evening, while at rest, in damp, wet weather, strong pressure.
Oxalic Acid: – Frequent and copious. Burning in urethra and pain in glans when urinating. Must urinate when thinking of it. Urine contains oxalates. Worse, left side; slightest touch; light; shaving. All conditions made worse by thinking about self.
SERUM-ANGUILLAE (Eel Serum):- presence of albumin and renal elements in the urine, the haemoglobinuria, the prolonged anuria (24 and 26 hours), Whenever the kidney becomes acutely affected, either from cold or infection or intoxication, and the attack is characterized by oliguria, anuria and albuminuria, efficacious to re-establish diuresis, and in rapidly arresting albuminuria. hypertension and oliguria, without oedema. cardiac uraemia. acute nephritis a frigorie; Subacute nephritis. Heart diseases, in cases of failure of compensation and impending asystole.
Terebinth: – Inflammation of kidneys, with haemorrhages-dark, passive, fetid. Bright’s disease preceded by dropsy (Goullon). Drowsiness and strangury. Strangury, with bloody urine. Scanty, suppressed, odor of violets. Urethritis, with painful erections. Inflamed kidneys following any acute disease. Constant tenesmus.
Thuja Occ:- Rapid exhaustion and emaciation. Left-sided and chilly medicine; Great Anti sycotic drug; Complains arise after suppressed gonorrhoea; Urethra swollen inflamed. Urinary stream split and small. Sensation of trickling after urinating. Severe cutting after. Frequent micturition accompanying pains. Desire sudden and urgent, but cannot be controlled. Paralysis sphincter vesicae. Worse, at night, from heat of bed; at 3 am and 3 pm; from cold, damp air; after breakfast; fat, coffee; vaccination. Better, left side; while drawing up a limb.
Urea Pura:- Renal dropsy, with symptoms of general intoxication; Albuminuria, diabetes; urćmia. Urine thin and of low specific gravity. A hydrogogue diuretic in the treatment of dropsies. 10 grains every 6 hours.
Urtica urens:- Useful in cases when there is high serum uric acid levals; gouty & rheumatic diathesis; Worse, from snow-air; water, cool moist air, touch.
Zinzibar off:- Complete cessation of function of kidneys. Frequent desire to urinate. Stinging, burning in orifice. Yellow discharge from urethra. Urine thick, turbid, of strong odor, suppressed. Complete suppression after typhoid. After urinating, continues to ooze in drops.
AKI: acute kidney injury; GFR: glomerular filtration rate; S.Cr: serum creatinine ; Ur: urea
UO: urine output;RRT: renal replacement therapy; Pmp: population per million; ITU: intensive treatment unit
ESRD: end stage renal disease; ATN: acute tubular necrosis; TIN: tubulointerstitial nephritis; GN: glomerulonephritis
NSAID: non steroidal anti-inflammatory drugs; ACE-I: angiotensin converting enzyme inhibitors; ARB: aldosterone receptor blocker
RBF: renal blood flow; NBM: nil by mouth; ECG: electrocardiogram; DIC: disseminated intravascular coagulation
LDH: lactic acid dehydrogenase; CBC: complete blood count
Na+ : sodium; K+: potassium; HCO3- : bicarbonate ion; PO4- : phosphate ion
LFT: liver function test
CRP: c- reactive protein
Bibliography: –
• Oxford Handbook of Nephrology and Hypertension;
Second edition ; Simon Steddon Consultant Nephrologist Guy’s and St Thomas’ Hospitals London, UK and Neil Ashman Consultant Nephrologist St Bartholomew’s and the Royal London Hospitals London, UK
With Alistair Chesser Consultant Nephrologist St Bartholomew’s and the Royal London Hospitals London, UK and John Cunningham Professor of Nephrology Royal Free & University College Hospitals London, UK; © Oxford University Press, 2014
• Harrison’s Principle of Internal Medicine, 20th edition-2018, volume 2, McGraw-Hill companies, Inc, United states of America.

• Boericke’s New Manual of Homeopathic Materia Medica with Repertory:
Third Revised & Augmented Edition Based on Ninth Edition
by Garth W. Boericke ,
by Oscar E. BOERICKE, M.D.
Publisher: B.Jain
• Organon of Medicine by Samual Hahnemann; R.E.Dudgeon
Publisher: B. Jain Low Priced; Fifth & Sixth edition (23 September 2013)
• Illustrated Guide to the Homeopathic Treatment: 3rd Edition by Harbans Singh Khaneja
Publisher: Health Harmony; Third edition (1 April 2012)

About the author

Dr Nidhi Dave

I am a M.D student. pursuing MD from ahmedabad homoeopathic medical college under guidence of Dr Heena Rawal in department of organon of medicine.