Other tests/analysis are:
High CK levels(x10-150 times normal)
MRI can indicate different types of LGMD. EMG can confirm the myopathic characteristic of the disease. Electrocardiography (cardiac arrhythmias in LGMD1B can occur)

Types
The "LGMD D" family is autosomal dominant, and the "LGMD R" family is autosomal recessive. Limb–girdle muscular dystrophy is explained in terms of gene, locus, OMIM and type as follows:

LGMD criteria
For a disease entity to be classified as an LGMD, the following criteria must be met:
genetic, with an identifiable inheritance pattern such as autosomal dominant, autosomal recessive, digenic, or polygenic. relatively selective to skeletal muscle
predominantly proximal muscle involvement
independent walking is achieved at one point in life
elevated serum creatine kinase
muscle fiber loss
dystrophic changes in muscle histology
degenerative changes on medical imaging
end-stage pathology seen in the most affected muscles
described in at least two unrelated families

Differential
Many diseases can manifest similarly to LGMD. Dystrophinopathies, including Duchenne muscular dystrophy, Becker muscular dystrophy, and manifesting dystrophinopathy in female carriers, can present similarly to LGMD. Facioscapulohumeral muscular dystrophy can appear similarly, especially when it spares the facial muscles. Also in the differential are Emery-Dreifuss muscular dystrophies, Pompe disease, later-onset congenital myasthenic syndromes, and proximal-predominant hereditary motor neuropathies. Treatment
There are few studies corroborating the effectiveness of exercise for limb–girdle muscular dystrophy. However studies have shown that exercise can, in fact, damage muscles permanently due to intense muscle contraction. Physical therapy may be required to maintain as much muscle strength and joint flexibility as possible. Calipers may be used to maintain mobility and quality of life.
Future treatment could be had by gene therapy through recombinant adeno-associated vectors.According to a review by Straub, et al., there are several research issues that need to be addressed: the rareness of the disease, poor understanding of the mechanism of LGMD R, and absence of patient cohorts, all contributing to lack of biomarkers for LGMD. The review goes on to state that animal models for LGMD R have been used to analyze therapeutic medications. Also, although prednisone has been used and has had positive effects on affected LGMD2 individuals, there is still no evidence of its effectiveness in trials that are placebo-controlled. See also
Muscle atrophy

References
Further reading
Cotta, Ana; Carvalho, Elmano; da-Cunha-Júnior, Antonio Lopes; Paim, Júlia Filardi; Navarro, Monica M.; Valicek, Jaquelin; Menezes, Miriam Melo; Nunes, Simone Vilela; Xavier Neto, Rafael (2014). "Common recessive limb girdle muscular dystrophies differential diagnosis: why and how?". Arquivos de Neuro-Psiquiatria. 72 (9): 721–734. doi:10.1590/0004-282X20140110. ISSN 0004-282X. PMID 25252238. Liu, Jian; Harper, Scott Q. (2012-08-01). "RNAi-based Gene Therapy for Dominant Limb Girdle Muscular Dystrophies". Current Gene Therapy. 12 (4): 307–314. doi:10.2174/156652312802083585. ISSN 1566-5232. PMC 4120526. PMID 22856606. ANGELINI, CORRADO; TASCA, ELISABETTA; NASCIMBENI, ANNA CHIARA; FANIN, MARINA (2014-12-01). "Muscle fatigue, nNOS and muscle fiber atrophy in limb girdle muscular dystrophy". Acta Myologica. 33 (3): 119–126. ISSN 1128-2460. PMC 4369848. PMID 25873780. == External links ==