Trench nephritis

Trench nephritis
Trench nephritis
Other names	War nephritis
Specialty	Nephrology ; Military medicine ;
Symptoms	Albuminuria, high blood pressure, swelling, casts in urine, difficulty breathing and bronchitis.
Risk factors	Trench warfare
Prognosis	Low mortality, long recovery, frequent relapses

Last updated February 15, 2024

Trench nephritis, also known as war nephritis, is a kidney infection, first recognised by medical officers as a new disease during the early part of the First World War and distinguished from the then-understood acute nephritis by also having bronchitis and frequent relapses. Trench nephritis was the major kidney problem of the war. The cause was not established at the time, treatments were ineffective, and the condition led to 35,000 British and 2,000 American casualties.

The term trench nephritis was coined by Nathan Raw and was first reported in the British Medical Journal in 1915 as affecting soldiers of the British Expeditionary Force in Flanders. Soldiers presented with sudden-onset albuminuria, casts in urine, high blood pressure, swelling of legs or face, headache, sore throat and difficulty breathing and bronchitis. Pathology suggested an underlying inflammation of the small blood vessels of the kidneys.

Later evidence showed that trench nephritis may have been due to hantavirus, carried by rodents.

Background

Before the First World War, kidney diseases had been described in medical textbooks by physicians including Sir William Osler in 1909 and Marcus Seymour Pembrey in 1913.^[3] In November 1914, in the early months of the First World War, there were four million men living in 4,000 miles (6,400 km) of trenches, with which three diseases came to be closely associated: trench fever, trench foot, and trench nephritis.^[4]

Indian soldiers in trenches, Gallipoli (1915)
British soldier in trenches, Somme (1916)
Canadian soldiers in trenches, Somme (1916)
Italian soldiers in trenches (1918)

First World War

Trench nephritis, a term coined by Nathan Raw,^[1] was first reported in soldiers of the British Expeditionary Force in Flanders in the British Medical Journal (BMJ) in 1915. The article included a list of possible causes, including influenza, metal poisoning, toxins as a result of constipation, or a type of beriberi. There was a wide spectrum of opinion on the origin of the condition. Some believed it was a result of scarlet fever. Thomas Oliver wrote authoritatively in the BMJ that exposure was a cause. The Germans had reported that the disease occurred in a particular division of their army among those soldiers who slept on pavement rather than those who slept on wooden boards.^[5]^[6] Thereafter, the Medical Research Council began to investigate the new disease at St Bartholomew's Hospital, and the findings were discussed during the Royal Society of Medicine meeting in February 1916, with Osler as one of the four key speakers.^[6] At the time, consensus held with some uncertainty that the then understood acute nephritis was due to toxins, not infection.^[6] That this was not the case with the newly found nephritis was debated in several medical journals.^[3] Further clarity on an infectious cause was clouded by the finding that some cases did occur in men who had not been in the trenches, urine and blood cultures did not show any infection, and the disease did not appear to spread to areas near the trenches.^[3]^[7]

Affected soldiers presented with sudden onset of albuminuria, high blood pressure, swelling of legs or face, headache, sore throat and difficulty breathing and bronchitis. Casts were seen in the urine.^[1]^[2] It was distinguished from acute nephritis by its prolonged course and subsequent frequent relapses.^[2] Pathology revealed narrowing of small blood vessels in the kidneys, capillary thrombi, and a proliferation of cells affecting the capillary lumen, suggesting an underlying inflammation of blood vessels.^[2]

The cause was not established during the war and therefore preventative measures were not implemented.^[2] Trench nephritis was ineffectively treated in the same way that acute nephritis had been treated before the war. Research into the condition was stopped in 1918.^[1]

Epidemiology

Along with other trench diseases such as trench foot and trench fever, trench nephritis contributed to 25% of the British Expeditionary Force's triage bed occupancy and was the major kidney problem of the First World War.^[2]^[8] The condition led to hundreds of deaths and 35,000 British and 2,000 American casualties.^[1]^[9] The mortality was low, but men took a long time to recover.^[1]

Significance

Hantavirus transmission Hantavirus.jpg — Hantavirus transmission

Trench warfare was significant in subsequent wars such as the Second World War, the Falklands War and the Gulf War.^[4] Of the trench diseases, trench foot made a reappearance in the British Army during the Falklands War in 1982.^[10] Trench fever has also been detected during peacetime in homeless alcoholic people and people with HIV.^[4] There has since been evidence that a rise in kidney disease during the American Civil War and the occurrence of First World War trench nephritis may have been due to the rodent-spread hantavirus.^[11]^[12] A similar kidney disease was reported in epidemic proportions in 1934 in Sweden.^[11]

Related Research Articles

Trench fever is a moderately serious disease transmitted by body lice. It infected armies in Flanders, France, Poland, Galicia, Italy, Macedonia, Mesopotamia, Russia and Egypt in World War I. Three noted cases during WWI were the authors J. R. R. Tolkien, A. A. Milne, and C. S. Lewis. From 1915 to 1918 between one-fifth and one-third of all British troops reported ill had trench fever while about one-fifth of ill German and Austrian troops had the disease. The disease persists among the homeless. Outbreaks have been documented, for example, in Seattle and Baltimore in the United States among injection drug users and in Marseille, France, and Burundi.

Orthohantavirus is a genus of single-stranded, enveloped, negative-sense RNA viruses in the family Hantaviridae within the order Bunyavirales. Members of this genus may be called orthohantaviruses or simply hantaviruses.

Kidney disease, or renal disease, technically referred to as nephropathy, is damage to or disease of a kidney. Nephritis is an inflammatory kidney disease and has several types according to the location of the inflammation. Inflammation can be diagnosed by blood tests. Nephrosis is non-inflammatory kidney disease. Nephritis and nephrosis can give rise to nephritic syndrome and nephrotic syndrome respectively. Kidney disease usually causes a loss of kidney function to some degree and can result in kidney failure, the complete loss of kidney function. Kidney failure is known as the end-stage of kidney disease, where dialysis or a kidney transplant is the only treatment option.

Leptospirosis is a blood infection caused by the bacteria Leptospira that can infect humans, dogs, rodents and many other wild and domesticated animals. Signs and symptoms can range from none to mild to severe. Weil's disease, the acute, severe form of leptospirosis, causes the infected individual to become jaundiced, develop kidney failure, and bleed. Bleeding from the lungs associated with leptospirosis is known as severe pulmonary haemorrhage syndrome.

Sweating sickness, also known as the sweats, English sweating sickness, English sweat or sudor anglicus in Latin, was a mysterious and contagious disease that struck England and later continental Europe in a series of epidemics beginning in 1485. Other major outbreaks of the English sweating sickness occurred in 1508, 1517, and 1528, with the last outbreak in 1551, after which the disease apparently vanished. The onset of symptoms was sudden, with death often occurring within hours. Sweating sickness epidemics were unique compared with other disease outbreaks of the time: whereas other epidemics were typically urban and long-lasting, cases of sweating sickness spiked and receded very quickly, and heavily affected rural populations. Its cause remains unknown, although it has been suggested that an unknown species of hantavirus was responsible.

Lupus nephritis is an inflammation of the kidneys caused by systemic lupus erythematosus (SLE), an autoimmune disease. It is a type of glomerulonephritis in which the glomeruli become inflamed. Since it is a result of SLE, this type of glomerulonephritis is said to be secondary, and has a different pattern and outcome from conditions with a primary cause originating in the kidney. The diagnosis of lupus nephritis depends on blood tests, urinalysis, X-rays, ultrasound scans of the kidneys, and a kidney biopsy. On urinalysis, a nephritic picture is found and red blood cell casts, red blood cells and proteinuria is found.

Viral pneumonia is a pneumonia caused by a virus. Pneumonia is an infection that causes inflammation in one or both of the lungs. The pulmonary alveoli fill with fluid or pus making it difficult to breathe. Pneumonia can be caused by bacteria, viruses, fungi or parasites. Viruses are the most common cause of pneumonia in children, while in adults bacteria are a more common cause.

Interstitial nephritis, also known as tubulointerstitial nephritis, is inflammation of the area of the kidney known as the renal interstitium, which consists of a collection of cells, extracellular matrix, and fluid surrounding the renal tubules. It is also known as intestinal nephritis because the clinical picture may include mesenteric lymphadenitis in some cases of acute pyelonephritis. More specifically, in case of recurrent urinary tract infection, secondary infection can spread to adjacent intestine. In addition to providing a scaffolding support for the tubular architecture, the interstitium has been shown to participate in the fluid and electrolyte exchange as well as endocrine functions of the kidney.

Acute proliferative glomerulonephritis is a disorder of the small blood vessels of the kidney. It is a common complication of bacterial infections, typically skin infection by Streptococcus bacteria types 12, 4 and 1 (impetigo) but also after streptococcal pharyngitis, for which it is also known as postinfectious glomerulonephritis (PIGN) or poststreptococcal glomerulonephritis (PSGN). It can be a risk factor for future albuminuria. In adults, the signs and symptoms of infection may still be present at the time when the kidney problems develop, and the terms infection-related glomerulonephritis or bacterial infection-related glomerulonephritis are also used. Acute glomerulonephritis resulted in 19,000 deaths in 2013, down from 24,000 deaths in 1990 worldwide.

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Andes orthohantavirus (ANDV), a species of Orthohantavirus, is a major causative agent of hantavirus cardiopulmonary syndrome (HCPS) and hantavirus pulmonary syndrome (HPS) in South America. It is named for the Andes mountains of Chile and Argentina, where it was first discovered. Originating in the reservoir of rodents, Andes orthohantavirus is easily transmitted to humans who come into contact with infected rodents or their fecal droppings. However, infected rodents do not appear ill, so there is no readily apparent indicator to determine whether the rodent is infected or not. Additionally, Andes orthohantavirus, specifically, is the only hantavirus that can be spread by human to human contact via bodily fluids or long-term contact from one infected individual to a healthy person.

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The Picardy sweat was an infectious disease of unknown cause and one of the only diseases that bears resemblance to the English sweating sickness. The Picardy sweat is also known as the miliary fever, suette des Picards in French, and picard'scher Schweiß,picard'sches Schweissfieber, or Frieselfieber in German. It appeared in the northern French province of Picardy in 1718. The Picardy sweat was mainly confined to the northwest part of France, particularly in the provinces of Seine-et-Oise, Bas Rhin, and Oise. Although the Picardy sweat began in Northern France, outbreaks also occurred in Germany, Belgium, Switzerland, Austria, and Italy. Between 1718 and 1874, 194 epidemics of the Picardy sweat were recorded. The last extensive outbreak was in 1906, which a French commission attributed to fleas from field mice. A subsequent case was diagnosed in 1918 in a soldier in Picardy.

Hantavirus hemorrhagic fever with renal syndrome (HFRS) is a group of clinically similar illnesses caused by species of hantaviruses. It is also known as Korean hemorrhagic fever and epidemic hemorrhagic fever. It is found in Europe, Asia, and Africa. The species that cause HFRS include Hantaan orthohantavirus, Dobrava-Belgrade orthohantavirus, Saaremaa virus, Seoul orthohantavirus, Puumala orthohantavirus and other orthohantaviruses. Of these species, Hantaan River virus and Dobrava-Belgrade virus cause the most severe form of the syndrome and have the highest morbidity rates. When caused by the Puumala virus, it is also called nephropathia epidemica. This infection is known as sorkfeber in Swedish, myyräkuume in Finnish, and musepest in Norwegian.

Hantavirus pulmonary syndrome (HPS) is one of two potentially fatal syndromes of zoonotic origin caused by species of hantavirus. These include Black Creek Canal virus (BCCV), New York orthohantavirus (NYV), Monongahela virus (MGLV), Sin Nombre orthohantavirus (SNV), and certain other members of hantavirus genera that are native to the United States and Canada.

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Hantaan orthohantavirus (HTNV) is an enveloped, single-stranded, negative-sense RNA virus species of Old World Orthohantavirus. It is the causative agent of Korean hemorrhagic fever in humans. It is named for the Hantan River in South Korea, and in turn lends the name to its genus Orthohantavirus and family Hantaviridae.

Thottopalayam thottimvirus, formerly Thottapalayam virus, (TMPV) is single-stranded, enveloped, negative-sense RNA virus species of the genus Thottimvirus in the Bunyavirales order. It is the first hantavirus to be isolated from a shrew. It was discovered in India in 1964.

Nova virus is a single-stranded, negative-sense, enveloped RNA virus with a trisegmented genome. It belongs to one of the most divergent lineages of the hantavirus group, which consists of zoonotic viruses belonging to the family Bunyaviridae. As of now, no human cases of infection have been reported.

References

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↑ D’Souza, Michael Hilary; Patel, Trushar R. (7 August 2020). "Biodefense Implications of New-World Hantaviruses". Frontiers in Bioengineering and Biotechnology. 8: 925. doi: 10.3389/fbioe.2020.00925 . ISSN 2296-4185. PMC 7426369 . PMID 32850756.
↑ Newman, Edmund N. C.; Johnstone, Penelope; Bridge, Hannah; Wright, Deborah; Jameson, Lisa; Bosworth, Andrew; Hatch, Rebecca; Hayward-Karlsson, Jenny; Osborne, Jane; Bailey, Mark S.; Green, Andrew (December 2014). "Seroconversion for infectious pathogens among UK military personnel deployed to Afghanistan, 2008-2011". Emerging Infectious Diseases. 20 (12): 2015–2022. doi:10.3201/eid2012.131830. ISSN 1080-6059. PMC 4257834 . PMID 25418685.
↑ Thompson, Julian (18 September 2014). "Falklands Conflict Gallery By Major General Julian Thompson". BBC. Retrieved 13 December 2020.
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