A saddle sore in humans is a skin ailment on the buttocks due to, or exacerbated by, horse riding or cycling on a bicycle saddle. It often develops in three stages:  skin abrasion, folliculitis (which looks like a small, reddish acne), and finally abscess. Because it most commonly starts with skin abrasion, it is desirable to reduce the factors which lead to skin abrasion. Some of these factors include:

Reducing the friction. In equestrian activities, friction is reduced with a proper riding position and using properly fitting clothing and equipment. In cycling, friction from bobbing or swinging motion while pedaling is reduced by setting the appropriate saddle height. Angle and fore/aft position can also play a role, and different cyclists have different needs and preferences in relation to this. Selecting an appropriate size and design of horse riding saddle or bicycle saddle. Wearing proper clothing. In bicycling, this includes cycling shorts, with chamois padding. For equestrian activity, long, closely fitted pants such as equestrian breeches or jodhpurs minimize chafing. For western riding, closely fitted jeans with no heavy inner seam, sometimes combined with chaps, are preferred. Padded cycling shorts worn under riding pants helps some equestrians, and extra padding, particularly sheepskin, on the seat of the saddle may help in more difficult situations such as long-distance endurance riding. Using petroleum jelly, chamois cream or lubricating gel to further reduce friction.If left untreated over an extended period of time, saddle sores may need to be drained by a physician.
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. Signs and symptoms
Among the signs and symptoms of acute proliferative glomerulonephritis are the following:

Hematuria
Oliguria
Edema
Hypertension
Fever (headache, malaise, anorexia, nausea.) Causes
Acute proliferative glomerulonephritis (post-streptococcal glomerulonephritis) is caused by an infection with streptococcus bacteria, usually three weeks after infection, usually of the pharynx or the skin, given the time required to raise antibodies and complement proteins. The infection causes blood vessels in the kidneys to develop inflammation, this hampers the renal organs ability to filter urine. Acute proliferative glomerulonephritis most commonly occurs in children. Pathophysiology
The pathophysiology of this disorder is consistent with an immune-complex-mediated mechanism, a type III hypersensitivity reaction. This disorder produces proteins that have different antigenic determinants, which in turn have an affinity for sites in the glomerulus. As soon as binding occurs to the glomerulus, via interaction with properdin, the complement is activated.