Fleming first used the purified penicillin to treat streptococcal meningitis in 1942. For the discovery, Fleming shared the 1945 Nobel Prize in Physiology or Medicine with Florey and Chain. Several semisynthetic penicillins are effective against a broader spectrum of bacteria: these include the antistaphylococcal penicillins, aminopenicillins and the antipseudomonal penicillins. Nomenclature
The term "penicillin" is defined as the natural product of Penicillium mould with antimicrobial activity. It was coined by Alexander Fleming on 7 March 1929 when he discovered the antibacterial property of Penicillium rubens. Fleming explained in his 1929 paper in the British Journal of Experimental Pathology that "to avoid the repetition of the rather cumbersome phrase Mould broth filtrate, the name penicillin will be used." The name thus refers to the scientific name of the mould, as described by Fleming in his Nobel lecture in 1945:I have been frequently asked why I invented the name "Penicillin". I simply followed perfectly orthodox lines and coined a word which explained that the substance penicillin was derived from a plant of the genus Penicillium just as many years ago the word "Digitalin" was invented for a substance derived from the plant Digitalis.In modern usage, the term penicillin is used more broadly to refer to any β-lactam antimicrobial that contains a thiazolidine ring fused to the β-lactam core, and may or may not be a natural product. Like most natural products, penicillin is present in Penicillium moulds as a mixture of active constituents (gentamicin is another example of a natural product that is an ill-defined mixture of active components).
Other consequences include arterial stiffening, which involves a gradual breakdown of elastic fibers and intima (the innermost layer of a blood vessel) thickening. Glomerular hypertension and glomerular hyperfiltration
An alternative mechanism of hypertensive nephropathy is prolonged glomerular hypertension and hence glomerular hyperfiltration. These can occur simultaneously but not necessarily. The idea is that hypertension results in sclerosis of the glomeruli which ultimately means reduced kidney function. As a compensatory mechanism, the unaffected nephrons (specifically, the preglomerular arterioles) vasodilate to increase blood flow to the kidney perfusion and increase glomerular filtration across undamaged glomeruli. Diagnosis
Diagnosis of HN is made from clinical history and biochemical investigations. Chronic hypertension with progressive kidney disease progresses over a long period of time. Damage to the glomeruli allows proteins that are usually too large to pass into the nephron to be filtered. This leads to an elevated concentration of albumin in the urine (albuminuria). This albuminuria usually does not cause symptoms but can be indicative of many kidney disorders. Protein in the urine (proteinuria) is best identified from a 24-hour urine collection.Bilateral renal artery stenosis should always be considered as a differential diagnosis for the presentation of HN. Kidney disease with this etiology can potentially be reversed following vascular intervention. Histology
In benign nephrosclerosis, the changes occurring are gradual and progressive, however, there can be sufficient kidney reserve capacity to maintain adequate kidney function for many years. The large renal arteries exhibit intimal thickening, medial hypertrophy, duplication of the elastic layer.