Nao Sha

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Sal ammoniac (NH4Cl)

Not yet clinically reviewed

Pinyin: Nao Sha
Salmonite Halite Sal

Traditionally used for

  • Eye health
  • Nose & throat
  • Cough & breathing
  • Digestion
  • Skin

Cautions & contraindications

  • Pregnancy
  • Kidney conditions
  • Toxic — professional use only
Moderate evidence · 2 studies

☯ TCM Properties

Category: external applications
Temperature: warm
Taste: salty, bitter
Meridians: liver, spleen, stomach
Functions:

Disperses Accumulation and stagnant Blood; Resolves Phlegm, promotes diuresis, softens hardness and removes film

Traditional Chinese Uses

Nao Sha is sal ammoniac, the mineral ammonium chloride (NH4Cl). Salty, bitter and pungent and warm (and toxic), entering the Liver, Spleen and Stomach channels, it disperses accumulations and Blood stasis, resolves Phlegm, softens hardness and removes decayed tissue and films. Traditionally it is used mainly externally: applied to abdominal masses and glandular swellings, to non-healing or necrotic sores and warts to slough dead tissue, and to eye conditions such as corneal opacity (nebula) and pterygium, as well as nasal polyps.

Given its toxicity and corrosive, irritant nature, it is used almost exclusively as an external application, crushed and prepared into pastes, powders or plasters; internal use is minimal, tightly dosed and avoided in pregnancy and in weak patients. It should not be applied to broad areas of broken skin.

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Botanical Description

Nao Sha, sal ammoniac, is a naturally occurring or refined mineral substance composed of ammonium chloride (NH4Cl). It crystallises in the isometric system as colourless to white, sometimes yellow- or grey-tinted cubes or fibrous aggregates, often found near volcanic fumaroles and burning coal seams. The drug has a sharp, salty, biting taste and is highly soluble in water. In classical TCM it is described as salty, bitter, acrid, and warm with toxicity, and was used to soften hardness, disperse accumulations, transform phlegm, eliminate damp, and expel parasites; topical applications include corrosive treatment of warts, fixed masses, and chronic ulcerations. Owing to potential mucosal irritation, gastrointestinal toxicity, and risk in patients with renal or hepatic impairment, modern Chinese practice discourages internal use and reserves it for carefully controlled external preparations.

Active Constituents

Ammonium chloride (NH4Cl)

Inorganic halide salt (ammonium salt of hydrochloric acid)

Concentration: The drug is essentially the pure salt; white nao sha (bai nao sha) is graded on its ammonium chloride content

A systemic acidifying agent. After absorption the ammonium ion is converted to urea in the liver, liberating hydrogen ion and leaving chloride behind, which produces a hyperchloraemic metabolic acidosis and an acid urine. The same acid load drives the expectorant effect by reflex gastric irritation and the mild osmotic diuresis of the chloride. Locally the concentrated salt is irritant and caustic, which underlies the classical use for corneal pannus and for dispersing masses.

Iron(III) and associated mineral impurities

Mineral impurities of the natural salt

Concentration: Trace; variable with the volcanic source of the crude mineral

Naturally occurring sal ammoniac forms by sublimation from volcanic exhalations and carries iron and other mineral impurities, which give the crude drug its colour. They have no established pharmacological role and are a quality rather than an activity consideration.

⚠ Drug Interactions

Memantine

Major Evidence: Established

Memantine is a weak base cleared largely unchanged by the kidney, and its renal handling is strongly pH-dependent. In a randomised four-period crossover study in 12 healthy men at steady state, renal clearance under acidified urine was 7 to 10 times higher than under alkalinised urine (median 210 versus 19 mL/min), and the amount excreted over 24 hours was 5.7 to 7.4 times higher. Ammonium chloride is one of the classical means of producing exactly that acidification, so a patient taking Nao Sha alongside memantine can lose most of the drug in the urine.

Clinical note: Do not give ammonium chloride, in any form including this herb, to a patient on memantine. The interaction is large enough to render the memantine ineffective, and the loss will not be obvious clinically until cognition deteriorates.

Amphetamine and dexamfetamine (and, by the same mechanism, other basic amines such as pseudoephedrine and quinidine)

Major Evidence: Established

Beckett and Rowland showed in humans that urinary pH governs amphetamine excretion: in acid urine the drug is ionised in the tubular lumen, cannot be reabsorbed, and is excreted rapidly. Ammonium chloride was for decades the standard agent used to produce this effect, and it was used therapeutically to accelerate amphetamine elimination in overdose. The same tubular trapping applies to other weak bases cleared renally, including pseudoephedrine, ephedrine, quinidine and flecainide.

Clinical note: Treat any renally cleared basic drug as at risk. Avoid Nao Sha in patients on stimulants for ADHD or on quinidine or flecainide, and remember that abrupt withdrawal of the acidifier can push levels back up as sharply as starting it pushed them down.

Aspirin and other salicylates

Major Evidence: Established

Salicylate is a weak acid whose renal elimination is exquisitely pH-sensitive: alkalinising the urine is a mainstay of salicylate poisoning treatment because it traps the ionised drug in the tubule. Acidifying the urine does the reverse, promoting non-ionic back-diffusion and reabsorption. Ammonium chloride therefore works directly against salicylate clearance, and the effect is amplified because the accompanying systemic acidosis shifts salicylate out of plasma into tissues, including the brain.

Clinical note: Never combine Nao Sha with regular salicylate therapy, and never give any acidifying agent to a patient with suspected salicylate toxicity. The systemic acidosis is as dangerous as the reduced clearance.

Spironolactone, eplerenone, amiloride and triamterene

Major Evidence: Probable

Potassium-sparing diuretics block distal sodium reabsorption, reduce the lumen-negative potential that drives potassium and hydrogen secretion, and so produce a type 4 hyperkalaemic distal renal tubular acidosis. Ammonium chloride imposes a fixed acid load on top of a kidney whose ability to excrete that acid has been pharmacologically impaired. The result is additive rather than merely coincident, and the acidosis itself worsens hyperkalaemia by shifting potassium out of cells.

Clinical note: Avoid the combination. If a patient on any potassium-sparing diuretic has taken a mineral prescription containing Nao Sha, check bicarbonate, chloride and potassium rather than assuming the salt is inert.

Methenamine (hexamine) hippurate and mandelate

Moderate Evidence: Established

Methenamine is a prodrug that only becomes antibacterial once hydrolysed to formaldehyde, and that hydrolysis requires an acid urine, conventionally below pH 6. Ammonium chloride was one of the standard adjuncts used to achieve it. The interaction is beneficial in intent, but it is still an interaction: the acid load is real and can be significant in an elderly patient with reduced renal reserve, and adding a herbal source of ammonium chloride on top of a prescribed acidifier can overshoot.

Clinical note: If a patient on methenamine is also taking Nao Sha, do not treat the herb as duplicative but harmless. Monitor serum bicarbonate, and avoid the pairing entirely alongside sulphonamides, with which acid urine risks crystalluria.

Acetazolamide and other carbonic anhydrase inhibitors

Moderate Evidence: Probable

Carbonic anhydrase inhibition causes renal bicarbonate wasting and a proximal renal tubular acidosis. Superimposing an exogenous acid load from ammonium chloride removes the compensatory reserve. The mechanisms are independent and the effect on serum bicarbonate is additive.

Clinical note: Avoid in patients on acetazolamide, topiramate or zonisamide, all of which carry carbonic anhydrase inhibitory activity.

Evidence Tier

Moderate evidence · 2 studies

Recorded studies by study design, strongest design at the top. This is a study-design tier only, not a GRADE rating: it does not weigh risk of bias, consistency or precision.

Systematic review / meta-analysis

0

Randomized controlled trial

1

1 verified · 0 unverified

Show the study

Other clinical trial

0

In vitro / animal

0

Other / unclassified

0

Verified: design read from PubMed for a DOI that resolves to the cited paper Unverified: taken from the study's recorded description

Clinical Studies

Influence of urine pH and urinary flow on the renal excretion of memantine

Freudenthaler S, Meineke I, Schreeb KH, Boakye E, Gundert-Remy U, Gleiter CH (1998) British Journal of Clinical Pharmacology RCT Verified: Randomized controlled trial

Twelve healthy men took memantine 10 mg daily for 43 days and, at steady state, went through four randomised crossover regimens combining acidified or alkalinised urine with low or high urine flow. Renal clearance under acid urine was 7 to 10 fold higher than under alkaline urine, and the 24-hour amount excreted was 5.7 to 7.4 fold higher, while urine flow had no clinically relevant effect. The authors concluded that anything altering urine pH should be avoided during memantine treatment. This is the strongest quantitative evidence available for why an ammonium chloride-containing drug matters clinically.

Selective screening for distal renal tubular acidosis in recurrent kidney stone formers: initial experience and comparison of the simultaneous furosemide and fludrocortisone test with the short ammonium chloride test

Shavit L, Chen L, Ahmed F, Ferraro PM, Moochhala S, Walsh SB, Unwin R (2016) Nephrology Dialysis Transplantation cohort

A clinical study using the short ammonium chloride loading test as a reference standard for diagnosing incomplete distal renal tubular acidosis in recurrent stone formers, compared against a furosemide plus fludrocortisone protocol. It is cited here not for a therapeutic claim but because it documents the physiological effect an ammonium chloride load reliably produces in humans: a measurable systemic acid load and urinary acidification. That predictable effect is precisely what makes Nao Sha pharmacologically active and what drives its interactions. Ammonium chloride loading is poorly tolerated, which is itself why nephrology has sought alternatives to it.

Historical Texts

Xin Xiu Ben Cao (Tang Ben Cao)

Tang dynasty (659)
Chinese sources give the Tang Ben Cao as the source text (chu chu) for nao sha. It is entered among the mineral drugs, salty, bitter and acrid in taste and warm in nature, used to disperse accumulations and masses, for choking diaphragm and stomach reflux, and topically for throat swelling and for corneal opacity and pterygium.

Ri Hua Zi Ben Cao

Five Dynasties to early Song (tenth century)
Records the synonym di yan, literally Di salt, reflecting the drug's arrival in China as an import along the northwestern trade routes. Other recorded synonyms, bei ting sha and rong nao, likewise name foreign places of origin rather than a Chinese source.

Traditional cautions recorded across the Chinese materia medica

Tang dynasty onward
Nao sha is consistently recorded as toxic and corrosive, contraindicated in pregnancy and in patients who are deficient and without accumulation or heat. The classical internal dose is only about 1 to 3 fen, roughly 0.3 to 1 g, with external use in appropriate amount as powder or in solution applied to the affected area.

References

  1. Beckett AH, Rowland M. INFLUENCE OF URINARY pH ON EXCRETION OF AMPHETAMINE . The Lancet (1965) [DOI]
  2. Proudfoot AT, Krenzelok EP, Brent J, Vale JA. Does Urine Alkalinization Increase Salicylate Elimination? If so, Why? . Toxicological Reviews (2003) [DOI]

This information is for educational purposes only and is not intended to replace professional medical advice. Always consult a qualified healthcare provider before using any herbal remedy, especially if you are pregnant, nursing, or taking medications.

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